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Loss of Kinesin KIF16B Disrupts Organelle Dynamics for Developmental Potential in Oocytes 激酶蛋白KIF16B的缺失破坏卵母细胞发育潜能的细胞器动力学。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202504857R
Meng-Xiang Li, Zi-Jian Wu, Kun-Huan Zhang, Yuan-Jing Zou, Ping-Shuang Lu, Shuo-Cheng Fan, Xuan Wu, Shao-Chen Sun, Yue Wang

Kinesin KIF16B, as a molecular motor protein within cells, primarily utilizes energy derived from ATP hydrolysis to transport intracellular cargo along microtubules, thereby participating in material transport, organelle dynamics, and cytoskeletal organization. However, the mechanism by which KIF16B regulates the maturation process of cytoplasm in mouse oocytes remains unclear. This study was to investigate the potential role of KIF16B in modulating organelle dynamics in mouse oocytes. Our findings suggest that depletion of KIF16B impairs oocyte developmental competence following parthenogenesis, implying potential abnormalities in oocyte maturation. We observed that oocytes with diminished KIF16B exhibited disrupted mitochondrial distribution and function, and further analysis revealed that this may be due to KIF16B involvement in p-Drp1 and Fis1-mediated mitochondrial fission. Besides, impaired mitochondrial function also resulted in oxidative stress. Additionally, abnormal distribution of the ER and ER stress were observed in oocytes lacking KIF16B. This was accompanied by elevated expression of ER stress-related genes CHOP and ATF4. Concurrently, KIF16B knockdown affected the distribution and function of the Golgi apparatus, leading to abnormalities in Golgi-based vesicular transport processes. In summary, our data suggest that the kinesin KIF16B modulates organelle dynamics during oocyte maturation.

{"title":"Loss of Kinesin KIF16B Disrupts Organelle Dynamics for Developmental Potential in Oocytes","authors":"Meng-Xiang Li,&nbsp;Zi-Jian Wu,&nbsp;Kun-Huan Zhang,&nbsp;Yuan-Jing Zou,&nbsp;Ping-Shuang Lu,&nbsp;Shuo-Cheng Fan,&nbsp;Xuan Wu,&nbsp;Shao-Chen Sun,&nbsp;Yue Wang","doi":"10.1096/fj.202504857R","DOIUrl":"10.1096/fj.202504857R","url":null,"abstract":"<div>\u0000 \u0000 <p>Kinesin KIF16B, as a molecular motor protein within cells, primarily utilizes energy derived from ATP hydrolysis to transport intracellular cargo along microtubules, thereby participating in material transport, organelle dynamics, and cytoskeletal organization. However, the mechanism by which KIF16B regulates the maturation process of cytoplasm in mouse oocytes remains unclear. This study was to investigate the potential role of KIF16B in modulating organelle dynamics in mouse oocytes. Our findings suggest that depletion of KIF16B impairs oocyte developmental competence following parthenogenesis, implying potential abnormalities in oocyte maturation. We observed that oocytes with diminished KIF16B exhibited disrupted mitochondrial distribution and function, and further analysis revealed that this may be due to KIF16B involvement in p-Drp1 and Fis1-mediated mitochondrial fission. Besides, impaired mitochondrial function also resulted in oxidative stress. Additionally, abnormal distribution of the ER and ER stress were observed in oocytes lacking KIF16B. This was accompanied by elevated expression of ER stress-related genes CHOP and ATF4. Concurrently, KIF16B knockdown affected the distribution and function of the Golgi apparatus, leading to abnormalities in Golgi-based vesicular transport processes. In summary, our data suggest that the kinesin KIF16B modulates organelle dynamics during oocyte maturation.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Bone Organ-on-a-Chip Uncovers That TPD52L1 Enhances Osteogenic Differentiation of MSCs and Contributes to Osteoporosis Repair 骨器官芯片揭示TPD52L1增强MSCs成骨分化并促进骨质疏松修复
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202503575RR
Zhewen Liu, Weina Ju, Fukun Lin, Yiming Liu, Baochang Qi

This study aims to develop a novel therapeutic strategy for osteoporosis (OP) by enhancing the osteogenic differentiation potential of mesenchymal stem cells (MSCs). A three-channel biomimetic bone organ-on-a-chip model was constructed. Through bioinformatics analysis, TPD52L1, a key upregulated gene involved in the osteogenic differentiation of MSCs, was identified. Molecular experiments were conducted to verify the effects of its overexpression on the Wnt/β-catenin pathway. Critically, systematic knockdown experiments were performed to validate its necessity in mechanotransduction. Subsequently, functional experiments were performed to evaluate its role in the osteogenic and adipogenic differentiation of MSCs in a GIOP model. Safety assessments for TPD52L1-overexpressing MSCs covered subcellular localization, proliferation, anchorage-independent growth, oncogene expression, and short-term in vivo tumorigenicity. TPD52L1 overexpression activated the Wnt/β-catenin pathway and promoted osteogenic differentiation of MSCs. Its knockdown blocked mechanical stimulation-induced pathway activation and osteogenic marker upregulation, confirming its necessity in mechano-osteogenic conversion. TPD52L1 upregulated osteoblast markers osteocalcin (OCN) and alkaline phosphatase (ALP), downregulated the osteoclast marker tartrate-resistant acid phosphatase (TRAP), and reversed the osteoporosis phenotype. When combined with cyclic mechanical force stimulation in the organ-on-a-chip system, a synergistic effect was observed, enhancing bone repair. TPD52L1 was localized in the cytoplasm, and its endogenous expression was upregulated by mechanical stimulation, indicating mechanosensitivity. TPD52L1 overexpression did not affect MSCs' proliferation, anchorage-independent growth, or oncogene expression. Subcutaneous transplantation experiments confirmed that it did not induce tumor formation or significant pathological changes, demonstrating favorable biosafety. TPD52L1 serves as a key target for promoting the osteogenic differentiation of MSCs.

{"title":"Bone Organ-on-a-Chip Uncovers That TPD52L1 Enhances Osteogenic Differentiation of MSCs and Contributes to Osteoporosis Repair","authors":"Zhewen Liu,&nbsp;Weina Ju,&nbsp;Fukun Lin,&nbsp;Yiming Liu,&nbsp;Baochang Qi","doi":"10.1096/fj.202503575RR","DOIUrl":"10.1096/fj.202503575RR","url":null,"abstract":"<div>\u0000 \u0000 <p>This study aims to develop a novel therapeutic strategy for osteoporosis (OP) by enhancing the osteogenic differentiation potential of mesenchymal stem cells (MSCs). A three-channel biomimetic bone organ-on-a-chip model was constructed. Through bioinformatics analysis, <i>TPD52L1</i>, a key upregulated gene involved in the osteogenic differentiation of MSCs, was identified. Molecular experiments were conducted to verify the effects of its overexpression on the Wnt/β-catenin pathway. Critically, systematic knockdown experiments were performed to validate its necessity in mechanotransduction. Subsequently, functional experiments were performed to evaluate its role in the osteogenic and adipogenic differentiation of MSCs in a GIOP model. Safety assessments for <i>TPD52L1-</i>overexpressing MSCs covered subcellular localization, proliferation, anchorage-independent growth, oncogene expression, and short-term in vivo tumorigenicity. <i>TPD52L1</i> overexpression activated the Wnt/β-catenin pathway and promoted osteogenic differentiation of MSCs. Its knockdown blocked mechanical stimulation-induced pathway activation and osteogenic marker upregulation, confirming its necessity in mechano-osteogenic conversion. <i>TPD52L1</i> upregulated osteoblast markers osteocalcin (OCN) and alkaline phosphatase (ALP), downregulated the osteoclast marker tartrate-resistant acid phosphatase (TRAP), and reversed the osteoporosis phenotype. When combined with cyclic mechanical force stimulation in the organ-on-a-chip system, a synergistic effect was observed, enhancing bone repair. <i>TPD52L1</i> was localized in the cytoplasm, and its endogenous expression was upregulated by mechanical stimulation, indicating mechanosensitivity. <i>TPD52L1</i> overexpression did not affect MSCs' proliferation, anchorage-independent growth, or oncogene expression. Subcutaneous transplantation experiments confirmed that it did not induce tumor formation or significant pathological changes, demonstrating favorable biosafety. TPD52L1 serves as a key target for promoting the osteogenic differentiation of MSCs.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Attenuation of Transforming Growth Factor-β Signaling Promotes Complete Recovery of Trabecular Bone Structure Following Immobilization With Traumatic Spinal Cord Injury 转化生长因子-β信号的衰减促进创伤性脊髓损伤固定后小梁骨结构的完全恢复。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202504448R
Karim Sahbani, Jeffry S. Nyman, Margo Button, Michael Hadjiargyrou, William A. Bauman, Hesham A. Tawfeek

Marked trabecular bone loss of the distal femoral and proximal tibial regions is one of the most common and devastating complications of spinal cord injury (SCI) with highest incidence of fracture and no efficacious treatment to date. Osteocytes exhibit increased transforming growth factor-β (TGF-β) signaling 5 weeks after SCI. Whether reducing TGF-β signaling will restore trabecular bone structure after development of bone loss with SCI has not been tested. To address this, male mice underwent laminectomy (sham) or thoracic (T10) contusion SCI resulting in complete hindlimb paralysis. Five weeks later, sham and SCI mice received either control (IgG) or anti-TGF-β neutralizing (ID11) antibody (10 mg/kg/day, twice weekly) for 5 weeks before sacrifice. Micro-computed tomography (micro-CT) analysis of the distal femoral region showed that, compared to sham-IgG animals, treatment with ID11 significantly (p < 0.05) restored trabecular fractional bone volume (107% SCI-ID11 vs. 65% SCI-IgG), thickness (109% SCI-ID11 vs. 88% SCI-IgG), connectivity (99% SCI-ID11 vs. 78% SCI-IgG), and structure model index (101% SCI-ID11 vs. 118% SCI-IgG). In contrast, analysis of femoral mid-shaft regions showed that both SCI-1D11 and SCI-IgG mice exhibited reduced cortical thickness (91% vs. 84%). Histomorphometric analysis revealed no differences in indices of osteoblast or osteoclast numbers or surfaces between SCI-IgG, SCI-1D11, and sham-IgG groups. Similarly, analysis of femoral bone marrow supernatants demonstrated no significant difference in levels of procollagen type 1 intact N-terminal propeptide (P1NP) or tartrate-resistant acid phosphatase 5b (TRAcP-5b). Thus, TGF-β signaling may be a promising therapeutic target to regain trabecular bone architecture and prevent fractures after SCI.

{"title":"Attenuation of Transforming Growth Factor-β Signaling Promotes Complete Recovery of Trabecular Bone Structure Following Immobilization With Traumatic Spinal Cord Injury","authors":"Karim Sahbani,&nbsp;Jeffry S. Nyman,&nbsp;Margo Button,&nbsp;Michael Hadjiargyrou,&nbsp;William A. Bauman,&nbsp;Hesham A. Tawfeek","doi":"10.1096/fj.202504448R","DOIUrl":"10.1096/fj.202504448R","url":null,"abstract":"<div>\u0000 \u0000 <p>Marked trabecular bone loss of the distal femoral and proximal tibial regions is one of the most common and devastating complications of spinal cord injury (SCI) with highest incidence of fracture and no efficacious treatment to date. Osteocytes exhibit increased transforming growth factor-β (TGF-β) signaling 5 weeks after SCI. Whether reducing TGF-β signaling will restore trabecular bone structure after development of bone loss with SCI has not been tested. To address this, male mice underwent laminectomy (sham) or thoracic (T10) contusion SCI resulting in complete hindlimb paralysis. Five weeks later, sham and SCI mice received either control (IgG) or anti-TGF-β neutralizing (ID11) antibody (10 mg/kg/day, twice weekly) for 5 weeks before sacrifice. Micro-computed tomography (micro-CT) analysis of the distal femoral region showed that, compared to sham-IgG animals, treatment with ID11 significantly (<i>p</i> &lt; 0.05) restored trabecular fractional bone volume (107% SCI-ID11 vs. 65% SCI-IgG), thickness (109% SCI-ID11 vs. 88% SCI-IgG), connectivity (99% SCI-ID11 vs. 78% SCI-IgG), and structure model index (101% SCI-ID11 vs. 118% SCI-IgG). In contrast, analysis of femoral mid-shaft regions showed that both SCI-1D11 and SCI-IgG mice exhibited reduced cortical thickness (91% vs. 84%). Histomorphometric analysis revealed no differences in indices of osteoblast or osteoclast numbers or surfaces between SCI-IgG, SCI-1D11, and sham-IgG groups. Similarly, analysis of femoral bone marrow supernatants demonstrated no significant difference in levels of procollagen type 1 intact N-terminal propeptide (P1NP) or tartrate-resistant acid phosphatase 5b (TRAcP-5b). Thus, TGF-β signaling may be a promising therapeutic target to regain trabecular bone architecture and prevent fractures after SCI.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Establishment and Functional Characterization of Bovine Endometrial Epithelial Organoids 牛子宫内膜上皮类器官的建立及功能表征。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202503351R
Iebu Devkota, Zachary L. Bonomo, Dailin M. Fuego, Yuxia Li, Xujia Zhang, Shavahn C. Loux, Charles R. Looney, Ana I. V. Maia, Fabrizio Donnarumma, Antonios Matsakas, Anastasios Vourekas, Philip H. Elzer, Xing Fu, Kenneth R. Bondioli, John J. Bromfield, Pablo Bermejo-Álvarez, Constantine A. Simintiras

Pre-implantation embryonic loss constitutes a major barrier to reproductive efficiency in livestock, yet the extrinsic determinants of embryonic survival remain poorly defined. Intra-organoid fluid (IOF) faithfully recapitulates native tissue secretions across multiple organ systems. We hypothesized that bovine endometrial epithelial organoids (BEEO) would produce IOF that mirrored in vivo uterine luminal fluid composition and extend embryo culture duration in vitro. We pursued three objectives: (a) establish and morphologically characterize BEEO, (b) define BEEO transcriptomic and secretory responses to 17β-estradiol (E2), medroxyprogesterone acetate (MPA), and interferon-tau (IFNτ), and (c) determine whether BEEO-derived IOF can support in vitro embryonic development beyond Day 8 (hatched blastocyst stage) under conventional culture conditions. BEEO were established from primary endometrial tissue (n = 4) and maintained a stable epithelial phenotype through multiple passages. Transcriptomic profiling revealed robust responses to stimulation, with E2, MPA, and IFNτ inducing distinct gene expression programs consistent with in vivo effects. IOF metabolomic analysis confirmed hormone-dependent regulation of IOF secretory output, with E2 + MPA (diestrus mimic) enhancing the production of metabolites implicated in conceptus development. Remarkably, IOF from diestrus mimic-stimulated BEEO, despite being diluted approximately seven-fold in PBS, maintained embryo survival rates comparable to optimized commercial medium and exceeded PBS-only controls. These findings position BEEO as a physiologically relevant model for dissecting maternal-embryo interactions in vitro and identifying targets to improve fertility in cattle and other livestock.

{"title":"Establishment and Functional Characterization of Bovine Endometrial Epithelial Organoids","authors":"Iebu Devkota,&nbsp;Zachary L. Bonomo,&nbsp;Dailin M. Fuego,&nbsp;Yuxia Li,&nbsp;Xujia Zhang,&nbsp;Shavahn C. Loux,&nbsp;Charles R. Looney,&nbsp;Ana I. V. Maia,&nbsp;Fabrizio Donnarumma,&nbsp;Antonios Matsakas,&nbsp;Anastasios Vourekas,&nbsp;Philip H. Elzer,&nbsp;Xing Fu,&nbsp;Kenneth R. Bondioli,&nbsp;John J. Bromfield,&nbsp;Pablo Bermejo-Álvarez,&nbsp;Constantine A. Simintiras","doi":"10.1096/fj.202503351R","DOIUrl":"10.1096/fj.202503351R","url":null,"abstract":"<div>\u0000 \u0000 <p>Pre-implantation embryonic loss constitutes a major barrier to reproductive efficiency in livestock, yet the extrinsic determinants of embryonic survival remain poorly defined. Intra-organoid fluid (IOF) faithfully recapitulates native tissue secretions across multiple organ systems. We hypothesized that bovine endometrial epithelial organoids (BEEO) would produce IOF that mirrored in vivo uterine luminal fluid composition and extend embryo culture duration in vitro. We pursued three objectives: (a) establish and morphologically characterize BEEO, (b) define BEEO transcriptomic and secretory responses to 17β-estradiol (E2), medroxyprogesterone acetate (MPA), and interferon-tau (IFNτ), and (c) determine whether BEEO-derived IOF can support in vitro embryonic development beyond Day 8 (hatched blastocyst stage) under conventional culture conditions. BEEO were established from primary endometrial tissue (<i>n</i> = 4) and maintained a stable epithelial phenotype through multiple passages. Transcriptomic profiling revealed robust responses to stimulation, with E2, MPA, and IFNτ inducing distinct gene expression programs consistent with in vivo effects. IOF metabolomic analysis confirmed hormone-dependent regulation of IOF secretory output, with E2 + MPA (diestrus mimic) enhancing the production of metabolites implicated in conceptus development. Remarkably, IOF from diestrus mimic-stimulated BEEO, despite being diluted approximately seven-fold in PBS, maintained embryo survival rates comparable to optimized commercial medium and exceeded PBS-only controls. These findings position BEEO as a physiologically relevant model for dissecting maternal-embryo interactions in vitro and identifying targets to improve fertility in cattle and other livestock.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SPP1+ Macrophage-POSTN+ Fibroblast-Endothelial Triad Dictates Immunotherapy Response in Bladder Cancer SPP1+巨噬细胞-后n +成纤维细胞内皮三联体决定膀胱癌的免疫治疗反应。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202504456RR
Hualin Chen, Yueqiang Peng, Zhigang Ji, Jie Dong

Although immunotherapy has shown promise in improving outcomes for bladder cancer (BCa) patients, treatment responses remain highly variable. A comparative examination of the tumor microenvironment (TME) between responders and non-responders may reveal key resistance mechanisms and identify potential therapeutic targets. We integrated spatial transcriptomics, single-cell RNA sequencing, and multiplexed immunofluorescence to characterize spatial structures within the TME that influence response to anti-PD-1 therapy in BCa patients. In non-responders, we observed an accumulation of stem-like malignant epithelial cells with high MYBL2 expression near the tumor boundary. Furthermore, we identified a spatial triad structure—composed of SPP1+ tumor-associated macrophages (TAMs), POSTN+ cancer-associated fibroblasts (CAFs), and endothelial cells—located at the tumor periphery. This structure was associated with T-cell exclusion and reduced efficacy of immune checkpoint blockade. In a preclinical model, inhibiting SPP1 enhanced the response to anti-PD-1 therapy, resulting in reduced CAF infiltration and increased recruitment of cytotoxic T cells. Our study reveals a triad cellular structure mediated by SPP1+ TAMs, POSTN+ CAFs, and endothelial cells that contribute to immunotherapy resistance in BCa. Targeting this structure, particularly through SPP1 blockade, represents a promising strategy to augment the efficacy of immune checkpoint inhibitors.

{"title":"SPP1+ Macrophage-POSTN+ Fibroblast-Endothelial Triad Dictates Immunotherapy Response in Bladder Cancer","authors":"Hualin Chen,&nbsp;Yueqiang Peng,&nbsp;Zhigang Ji,&nbsp;Jie Dong","doi":"10.1096/fj.202504456RR","DOIUrl":"10.1096/fj.202504456RR","url":null,"abstract":"<div>\u0000 \u0000 <p>Although immunotherapy has shown promise in improving outcomes for bladder cancer (BCa) patients, treatment responses remain highly variable. A comparative examination of the tumor microenvironment (TME) between responders and non-responders may reveal key resistance mechanisms and identify potential therapeutic targets. We integrated spatial transcriptomics, single-cell RNA sequencing, and multiplexed immunofluorescence to characterize spatial structures within the TME that influence response to anti-PD-1 therapy in BCa patients. In non-responders, we observed an accumulation of stem-like malignant epithelial cells with high MYBL2 expression near the tumor boundary. Furthermore, we identified a spatial triad structure—composed of SPP1<sup>+</sup> tumor-associated macrophages (TAMs), POSTN<sup>+</sup> cancer-associated fibroblasts (CAFs), and endothelial cells—located at the tumor periphery. This structure was associated with T-cell exclusion and reduced efficacy of immune checkpoint blockade. In a preclinical model, inhibiting SPP1 enhanced the response to anti-PD-1 therapy, resulting in reduced CAF infiltration and increased recruitment of cytotoxic T cells. Our study reveals a triad cellular structure mediated by SPP1<sup>+</sup> TAMs, POSTN<sup>+</sup> CAFs, and endothelial cells that contribute to immunotherapy resistance in BCa. Targeting this structure, particularly through SPP1 blockade, represents a promising strategy to augment the efficacy of immune checkpoint inhibitors.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cholesterol Lowering Alone Fails to Reverse Atherosclerotic Plaque Necrosis, Granulopoiesis, and Neurovascular Neutrophils in Middle-Aged Mice 单独降低胆固醇不能逆转中年小鼠动脉粥样硬化斑块坏死、颗粒生成和神经血管中性粒细胞。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-07 DOI: 10.1096/fj.202503638RR
Olivia Gannon, Allison Rahtes, Jesse L. Bonin, Ignacia Salfate del Rio, Jessica Partridge, Christina Nickerson, Sayeed Khan, Ariana Nobles, Gideon R. Covert, Amber Bahr, Ramon Bossardi Ramos, Katherine C. MacNamara, Gabrielle Fredman

Cholesterol lowering through diet, lifestyle, and pharmacologic therapy remains central for limiting atherosclerosis and prevention of major adverse cardiovascular events. Yet, 33%–50% of individuals on lipid-lowering therapy continue to exhibit elevated inflammation. Middle age (MA) represents a critical window for disease acceleration, underscoring a need to better understand nonresolving inflammation in this time frame. Here, we rendered young (2 months) and MA mice (10 months) hypercholesterolemic with an AAV8-PCSK9 virus and western diet (WD). Following 20 weeks on WD, mice were switched to a chow diet for 6 weeks to induce lipid lowering. This design models dietary cholesterol reduction to dissect lipid-driven versus inflammation-driven pathways in atherosclerosis. At baseline atherosclerosis, we found that MA mice had increased plaque necrosis as well as increased circulating and bone marrow PMN compared to young mice. After chow switch, unlike in young mice, MA mice had increased plaque necrosis and reduced remodeling, as well as increased circulating white blood cells and bone marrow hematopoietic stem cell progenitors (HSPCs). In MA chow-switched mice, circulating neutrophils correlated with necrosis whereas young mice exhibited no correlation. Furthermore, MA atherosclerotic mice had bone marrow HSPCs and neutrophils that exhibited a more activated phenotype relative to young after chow switch. In addition, we observed elevated neutrophil–endothelial contacts in the hippocampal vasculature of MA mice after chow switch. While dietary intervention and lowered plasma cholesterol restrained atheroprogression in young, it was inadequate in MA mice, failing to reduce systemic inflammation and indicating the need for complementary therapies during this time frame.

{"title":"Cholesterol Lowering Alone Fails to Reverse Atherosclerotic Plaque Necrosis, Granulopoiesis, and Neurovascular Neutrophils in Middle-Aged Mice","authors":"Olivia Gannon,&nbsp;Allison Rahtes,&nbsp;Jesse L. Bonin,&nbsp;Ignacia Salfate del Rio,&nbsp;Jessica Partridge,&nbsp;Christina Nickerson,&nbsp;Sayeed Khan,&nbsp;Ariana Nobles,&nbsp;Gideon R. Covert,&nbsp;Amber Bahr,&nbsp;Ramon Bossardi Ramos,&nbsp;Katherine C. MacNamara,&nbsp;Gabrielle Fredman","doi":"10.1096/fj.202503638RR","DOIUrl":"10.1096/fj.202503638RR","url":null,"abstract":"<div>\u0000 \u0000 <p>Cholesterol lowering through diet, lifestyle, and pharmacologic therapy remains central for limiting atherosclerosis and prevention of major adverse cardiovascular events. Yet, 33%–50% of individuals on lipid-lowering therapy continue to exhibit elevated inflammation. Middle age (MA) represents a critical window for disease acceleration, underscoring a need to better understand nonresolving inflammation in this time frame. Here, we rendered young (2 months) and MA mice (10 months) hypercholesterolemic with an AAV8-PCSK9 virus and western diet (WD). Following 20 weeks on WD, mice were switched to a chow diet for 6 weeks to induce lipid lowering. This design models dietary cholesterol reduction to dissect lipid-driven versus inflammation-driven pathways in atherosclerosis. At baseline atherosclerosis, we found that MA mice had increased plaque necrosis as well as increased circulating and bone marrow PMN compared to young mice. After chow switch, unlike in young mice, MA mice had increased plaque necrosis and reduced remodeling, as well as increased circulating white blood cells and bone marrow hematopoietic stem cell progenitors (HSPCs). In MA chow-switched mice, circulating neutrophils correlated with necrosis whereas young mice exhibited no correlation. Furthermore, MA atherosclerotic mice had bone marrow HSPCs and neutrophils that exhibited a more activated phenotype relative to young after chow switch. In addition, we observed elevated neutrophil–endothelial contacts in the hippocampal vasculature of MA mice after chow switch. While dietary intervention and lowered plasma cholesterol restrained atheroprogression in young, it was inadequate in MA mice, failing to reduce systemic inflammation and indicating the need for complementary therapies during this time frame.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Limonin Is a Novel Hexokinase 2 Inhibitor That Suppresses Hepatic Stellate Cell Activation and Histone Lactylation 柠檬苦素是一种抑制肝星状细胞活化和组蛋白乳酸化的新型己糖激酶2抑制剂。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-06 DOI: 10.1096/fj.202504035R
Tian Lan, Chen-chen Wang, Jun-jie Ying, Wen Wang, Xi-xi Zeng, Wei-li Mao, Tao Lu, Si-wei Wang

Hexokinase 2 (HK2) is a pivotal enzyme in glycolytic metabolism and plays a crucial role in the activation of hepatic stellate cells (HSCs). Despite its importance, specific inhibitors targeting HK2 are still lacking in clinical practice. In this study, we utilized a human protein microarray to identify a significant interaction between limonin (Lim) and HK2. Subsequent analyses confirmed that Lim effectively inhibits HK2 activity and the modification of histone lactylation. Moreover, Lim's systemic effects include the downregulation of gene expression associated with HSC activation, which is closely linked to its modulation of HK2 and histone lactylation. Additionally, Lim exhibits anti-fibrotic properties, influencing the expression of genes involved in HSC activation and histone lactylation in vivo. These findings provide novel mechanistic insights into how Lim derivatives may mitigate hepatic fibrosis through the suppression of HK2 and targeted regulation of histone lactylation in activated HSCs.

{"title":"Limonin Is a Novel Hexokinase 2 Inhibitor That Suppresses Hepatic Stellate Cell Activation and Histone Lactylation","authors":"Tian Lan,&nbsp;Chen-chen Wang,&nbsp;Jun-jie Ying,&nbsp;Wen Wang,&nbsp;Xi-xi Zeng,&nbsp;Wei-li Mao,&nbsp;Tao Lu,&nbsp;Si-wei Wang","doi":"10.1096/fj.202504035R","DOIUrl":"10.1096/fj.202504035R","url":null,"abstract":"<div>\u0000 \u0000 <p>Hexokinase 2 (HK2) is a pivotal enzyme in glycolytic metabolism and plays a crucial role in the activation of hepatic stellate cells (HSCs). Despite its importance, specific inhibitors targeting HK2 are still lacking in clinical practice. In this study, we utilized a human protein microarray to identify a significant interaction between limonin (Lim) and HK2. Subsequent analyses confirmed that Lim effectively inhibits HK2 activity and the modification of histone lactylation. Moreover, Lim's systemic effects include the downregulation of gene expression associated with HSC activation, which is closely linked to its modulation of HK2 and histone lactylation. Additionally, Lim exhibits anti-fibrotic properties, influencing the expression of genes involved in HSC activation and histone lactylation in vivo. These findings provide novel mechanistic insights into how Lim derivatives may mitigate hepatic fibrosis through the suppression of HK2 and targeted regulation of histone lactylation in activated HSCs.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cardiac Circ-ZNF609 Inhibition Attenuates Doxorubicin-Induced Cardiotoxicity Without Affecting the Chemotherapeutic Efficacy of Doxorubicin on Cancer in Female Mice 抑制心脏Circ-ZNF609可减轻阿霉素诱导的雌性小鼠心脏毒性,但不影响阿霉素对癌症的化疗效果。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-06 DOI: 10.1096/fj.202503974R
Shuang Zhang, Xiaotong Ding, Yunwei Xu, Caiyue Cui, Yuchao Yang, Yuhan Shao, Tianhui Wang, Yihua Bei, Lijun Wang, Jiahong Xu

The cardiac burden associated with doxorubicin (DOX) significantly limits its application in cancer treatment. Therefore, it is essential to identify effective strategies to protect the heart from cardiotoxic damage caused by chemotherapy. As sex is among the risk factors associated with DOX-induced cardiotoxicity, whether the cardiac beneficial effects observed from male mice can be applied to female mice remains unknown. We established a two-week DOX-induced cardiotoxicity model, in which the cumulative DOX dose administered to mice was comparable to that used in previous research. This model effectively induces cardiotoxicity and fibrosis while allowing for a sufficiently long monitoring period to evaluate the chemotherapeutic effects of DOX on tumors, without imposing an excessive physiological burden on the mice from prolonged tumor growth. Utilizing this tumor-bearing murine model, we employed TC-1 cancer cells, which express HPV16-E6 and HPV16-E7 proteins, to investigate the cardioprotective effects of circ-ZNF609 inhibition in DOX-treated tumor-bearing female mice. Our findings indicate that cardiac inhibition of circ-ZNF609 protects against DOX-induced cardiotoxicity without compromising the anti-tumor efficacy of DOX in females. These results suggest that targeting circ-ZNF609 in the heart may represent a promising and viable therapeutic strategy for preventing DOX-induced cardiotoxicity.

{"title":"Cardiac Circ-ZNF609 Inhibition Attenuates Doxorubicin-Induced Cardiotoxicity Without Affecting the Chemotherapeutic Efficacy of Doxorubicin on Cancer in Female Mice","authors":"Shuang Zhang,&nbsp;Xiaotong Ding,&nbsp;Yunwei Xu,&nbsp;Caiyue Cui,&nbsp;Yuchao Yang,&nbsp;Yuhan Shao,&nbsp;Tianhui Wang,&nbsp;Yihua Bei,&nbsp;Lijun Wang,&nbsp;Jiahong Xu","doi":"10.1096/fj.202503974R","DOIUrl":"10.1096/fj.202503974R","url":null,"abstract":"<div>\u0000 \u0000 <p>The cardiac burden associated with doxorubicin (DOX) significantly limits its application in cancer treatment. Therefore, it is essential to identify effective strategies to protect the heart from cardiotoxic damage caused by chemotherapy. As sex is among the risk factors associated with DOX-induced cardiotoxicity, whether the cardiac beneficial effects observed from male mice can be applied to female mice remains unknown. We established a two-week DOX-induced cardiotoxicity model, in which the cumulative DOX dose administered to mice was comparable to that used in previous research. This model effectively induces cardiotoxicity and fibrosis while allowing for a sufficiently long monitoring period to evaluate the chemotherapeutic effects of DOX on tumors, without imposing an excessive physiological burden on the mice from prolonged tumor growth. Utilizing this tumor-bearing murine model, we employed TC-1 cancer cells, which express HPV16-E6 and HPV16-E7 proteins, to investigate the cardioprotective effects of circ-ZNF609 inhibition in DOX-treated tumor-bearing female mice. Our findings indicate that cardiac inhibition of circ-ZNF609 protects against DOX-induced cardiotoxicity without compromising the anti-tumor efficacy of DOX in females. These results suggest that targeting circ-ZNF609 in the heart may represent a promising and viable therapeutic strategy for preventing DOX-induced cardiotoxicity.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to “Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype” 更正“肺功能GWAS SNV rs12477314 (2q37.3)标记的基因组位点作为全身性炎症表型的调控区域”。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-06 DOI: 10.1096/fj.202600409

Grech, G.M., Fawcett, K.A., Hall, R.J., Grech, G., Ellul-Micallef, R., Hall, I.P. and Fenech, A.G. (2025), Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype. The FASEB Journal 39 (2025): e70689, https://doi.org/10.1096/fj.202403208R.

In paragraph 2 of section 2.3 | PheWAS Analysis and Protein Association Analysis, the text “Association between rs12477314 C>T and protein levels were tested assuming an additive genetic model” should have read: “Association between rs12477314 C>T and protein levels were tested in individuals of European ancestry assuming an additive genetic model and adjusting for Olink batch, age, sex, genotyping array and the first 10 ancestry-based PCs.”

In the Acknowledgements section, we omitted:

“UK Biobank analyses were conducted using the UK Biobank Resource under Application Numbers 648 and 43027.”

We apologize for these errors.

{"title":"Correction to “Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype”","authors":"","doi":"10.1096/fj.202600409","DOIUrl":"10.1096/fj.202600409","url":null,"abstract":"<p>Grech, G.M., Fawcett, K.A., Hall, R.J., Grech, G., Ellul-Micallef, R., Hall, I.P. and Fenech, A.G. (2025), Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype. <i>The FASEB Journal</i> 39 (2025): e70689, https://doi.org/10.1096/fj.202403208R.</p><p>In paragraph 2 of section <b>2.3 | PheWAS Analysis and Protein Association Analysis</b>, the text “Association between rs12477314 C&gt;T and protein levels were tested assuming an additive genetic model” should have read: “Association between rs12477314 C&gt;T and protein levels were tested in individuals of European ancestry assuming an additive genetic model and adjusting for Olink batch, age, sex, genotyping array and the first 10 ancestry-based PCs.”</p><p>In the <b>Acknowledgements</b> section, we omitted:</p><p>“UK Biobank analyses were conducted using the UK Biobank Resource under Application Numbers 648 and 43027.”</p><p>We apologize for these errors.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://faseb.onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202600409","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Characterization of Transcriptional, Epigenetic, and Phenotypic Plasticity and Discovery of Biomarkers in Acute and Chronic Murine Schistosomiasis Infection 急性和慢性小鼠血吸虫病感染中转录、表观遗传和表型可塑性的表征以及生物标志物的发现。
IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-05 DOI: 10.1096/fj.202502913R
Sheila de Andrade Penteado Corrêa, Cauã da Silva Oliveira Teodoro, João Paulo Luz da Silva, Fabio Queiroz, Tayná Dandara do Amaral, Silmara Marques Allegretti, Fernanda Silva de Oliveira, Rafaela Ferraz Teixeira, Lizandra Maia de Sousa, Sílvio Roberto Consonni, Matheus de Souza Gomes, Christoph Grunau, Fernanda Janku Cabral

Parasites can induce changes in their hosts, favoring the success of the infection and its development at each stage of their life cycle. The host minimizes the effects of the parasite's presence through its defense system, balancing the parasite–host relationship. The intricate parasite–host relationship provides physiological, immunological, and molecular cues that suggest interaction and mutual regulation of the transcriptome and epigenome, promoting phenotypic plasticity and survival in a changing environment. There has been a growing interest in the epigenetic mechanisms of Schistosoma mansoni, a parasite with remarkable phenotypic plasticity in response to signals from the environment and its hosts. Several studies emphasize the epigenetic mechanisms behind the phenotypic plasticity of Schistosoma. Regarding the host's gene expression in the face of infection, however, there is little evidence of which pathways are altered by the passage of the parasite through the lungs and by the pathogenesis in the hepatic portal system. In this work, we characterized S. mansoni infection in parasitological and biochemical aspects of the murine model in comparison with the profile of the initial, acute, and chronic phases of infection (3, 7, and 20 wpi (weeks postinfection), respectively). The biochemical and morphological results of the infection at 3, 7, and 20 wpi show the phenotypic changes of schistosomiasis in the murine model. ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) at 7 wpi shows a chromatin with higher accessibility for infected individuals, and Western blotting at 7 wpi shows an increase in histone marks H3K9ac and H3K9me3, indicating a change in chromatin status after infection. RNA-seq (RNA sequencing) for 7 wpi results show a differential profile of lipid metabolism genes that are negatively modulated, while immune system genes are positively modulated. It is interesting to note that the negative modulation of mRNA expression of lipid pathway genes causes the rates of these metabolites to appear decreased in the blood, while the increased expression of immune system defense genes is in accordance with liver histology data, which shows an inflammatory profile.

{"title":"Characterization of Transcriptional, Epigenetic, and Phenotypic Plasticity and Discovery of Biomarkers in Acute and Chronic Murine Schistosomiasis Infection","authors":"Sheila de Andrade Penteado Corrêa,&nbsp;Cauã da Silva Oliveira Teodoro,&nbsp;João Paulo Luz da Silva,&nbsp;Fabio Queiroz,&nbsp;Tayná Dandara do Amaral,&nbsp;Silmara Marques Allegretti,&nbsp;Fernanda Silva de Oliveira,&nbsp;Rafaela Ferraz Teixeira,&nbsp;Lizandra Maia de Sousa,&nbsp;Sílvio Roberto Consonni,&nbsp;Matheus de Souza Gomes,&nbsp;Christoph Grunau,&nbsp;Fernanda Janku Cabral","doi":"10.1096/fj.202502913R","DOIUrl":"10.1096/fj.202502913R","url":null,"abstract":"<p>Parasites can induce changes in their hosts, favoring the success of the infection and its development at each stage of their life cycle. The host minimizes the effects of the parasite's presence through its defense system, balancing the parasite–host relationship. The intricate parasite–host relationship provides physiological, immunological, and molecular cues that suggest interaction and mutual regulation of the transcriptome and epigenome, promoting phenotypic plasticity and survival in a changing environment. There has been a growing interest in the epigenetic mechanisms of <i>Schistosoma mansoni</i>, a parasite with remarkable phenotypic plasticity in response to signals from the environment and its hosts. Several studies emphasize the epigenetic mechanisms behind the phenotypic plasticity of <i>Schistosoma</i>. Regarding the host's gene expression in the face of infection, however, there is little evidence of which pathways are altered by the passage of the parasite through the lungs and by the pathogenesis in the hepatic portal system. In this work, we characterized <i>S. mansoni</i> infection in parasitological and biochemical aspects of the murine model in comparison with the profile of the initial, acute, and chronic phases of infection (3, 7, and 20 wpi (weeks postinfection), respectively). The biochemical and morphological results of the infection at 3, 7, and 20 wpi show the phenotypic changes of schistosomiasis in the murine model. ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) at 7 wpi shows a chromatin with higher accessibility for infected individuals, and Western blotting at 7 wpi shows an increase in histone marks H3K9ac and H3K9me3, indicating a change in chromatin status after infection. RNA-seq (RNA sequencing) for 7 wpi results show a differential profile of lipid metabolism genes that are negatively modulated, while immune system genes are positively modulated. It is interesting to note that the negative modulation of mRNA expression of lipid pathway genes causes the rates of these metabolites to appear decreased in the blood, while the increased expression of immune system defense genes is in accordance with liver histology data, which shows an inflammatory profile.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12875175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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