Tissue & cell最新文献_第4页

Isolation and characterization of a new SHED cell line as a standard source for stem cell research and clinical translation.

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-30 DOI: 10.1016/j.tice.2024.102649

Niloufar Hosseini, Ezatolah Kazeminejad, Morteza Oladnabi, Ayyoob Khosravi

Background and aims: Stem cells from human exfoliated deciduous teeth (SHED) are multi-potent mesenchymal stem/stromal cells (MSCs) and are inspected a favorable, non-invasive source beneficial to stem cell-mediated regeneration of damaged tissues. Our aim was to establish and characterize a non-immortalized SHED cell line as an accessible resource and novel platform for stem cell research and tissue regeneration studies.

Methods: A Healthy exfoliated deciduous molar was extracted from a 12-year-old girl and shipped to an animal cell culture laboratory. Outgrowing primary cells from explanted small pulp tissues were monitored daily and characterized after passage 3 both morphologically and functionally. The SHED cell line was characterized by calculation of doubling time, cytogenetic analyses, STR analysis, adherence to cell culture flasks under standard cell culture media, and immunophenotypic analysis of specific MSC markers (CD90+, CD73+, CD34- and CD45-) using flow cytometry method. Differentiation potential to osteoblast, adipocyte, and chondrocyte was evaluated under standard differentiation media Expression of OCT-4 and NANOG genes was also assessed using RT-PCR method.

Results: After the third day, SHED cells were visible. SHED cells were subcultured when they reached 90 % confluence after approximately 17 days. The doubling time of SHED cells was forty seven hours. SHED immunophenotyping showed the high expression level of CD90 (99.2 %) and CD73 (45.9 %), and approximately no expression of CD34 (0.079 %) and CD45 (0.19 %). The human origin, female gender and chromosomal normality of SHED cells was confirmed by cytogenetic analysis. The STR matching analysis showed that SHED cells are well-identified and authentic. No genetic instability and cross-contamination were observed in SHED cells.

Conclusions: This study provides a new SHED cell line with a normal karyotype and all the characteristics of MSCs, which can be used as a favorable model cell line in biomedical research and a promising source for clinical translation.

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引用次数: 0

DLX4 promotes the expression of PD-L1 through GATA1 in Gestational Trophoblastic Neoplasia.

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-29 DOI: 10.1016/j.tice.2024.102641

Ying Wei, Chen Chen Zhu, Jiamu Xu, Weiping Hu, Jing Zhu

Gestational Trophoblastic Neoplasia (GTN) is a highly malignant tumor that originates from trophoblastic cells during embryonic development. In this study, we observed that DLX4, a member of the Distal-Less Homeobox (Dlx) gene family, was upregulated in GTN tissues and cell lines. Bioinformatic analysis showed that DLX4 was highly expressed in most cancers and had a poor survival prognosis in certain tumors; further analysis showed that DLX4 was significantly associated with genes of immune pathways and immune infiltration. Functional analyses revealed that DLX4 overexpression or knockdown did not affect GTN cell proliferation; however, we observed that DLX4 could regulate PD-L1 expression via GATA1. The luciferase reporter activity of the wild-type construct increased after overexpression of GATA1, whereas the mutation of the binding sites abolished the transcriptional increase. In conclusion, our findings suggest that DLX4 regulates PD-L1 expression via GATA1 in GTN and may be a new target for antitumor therapy.

引用次数: 0

NOX4 deficiency improves the impaired viability, inhibited the apoptosis and suppressed autophagy of DHEA-treated ovarian granulosa cells through inhibiting endoplasmic reticulum stress via inactivating PERK/ATF4 pathway

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-28 DOI: 10.1016/j.tice.2024.102640

Na Yu , Lingyuan Wu , Xin Xing

Background

PCOS is the most prevalent endocrine and metabolic problem in women of reproductive age. This current study was formulated to thoroughly expound the ovary-protecting effects of NOX4 deficiency in PCOS and probe into the intrinsic mechanisms underlying the protective effects of NOX4 deficiency against DHEA injury in ovarian GCs.

Methods

KGN cells were subjected to 20 nM DHEA for 48 h to establish PCOS cellular model. For loss-of-function experiments, KGN cells were transfected with si-NOX4. In addition, to investigate the biological roles of ERS and PERK/ATF4 pathway in the ovary-protecting effects of NOX4 deficiency in DHEA-treated ovarian GCs, KGN cells were pretreated with ERS agonist TM or PERK agonist CCT020312.

Results

NOX4 was highly expressed in DHEA-treated ovarian GCs. NOX4 deficiency improved the impaired viability, inhibited the apoptosis and suppressed autophagy of DHEA-treated ovarian GCs. Besides, NOX4 deficiency inactivated PERK/ATF4 pathway in DHEA-treated ovarian GCs. NOX4 deficiency repressed DHEA-induced ERS of ovarian GCs through inactivating PERK/ATF4 pathway. Pretreatment with ERS agonist TM or pretreatment with PERK agonist CCT020312 can both reduced the viability, promoted the apoptosis and strengthened autophagy of ovarian GCs, partially abolishing the ovary-protecting effects of NOX4 deficiency in DHEA-treated ovarian GCs. In general, NOX4 deficiency could improve the impaired viability, inhibited the apoptosis and suppressed autophagy of DHEA-treated ovarian GCs through repressing ERS depending on inactivation of PERK/ATF4 pathway.

Conclusion

To conclude, downregulation of NOX4 could exert ovary-protecting effects in DHEA-induced PCOS cellular model through repressing ERS via inactivating PERK/ATF4 pathway.

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引用次数: 0

The Shh-p38-NFATc1 signaling pathway is essential for osteoclastogenesis during tooth eruption

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-28 DOI: 10.1016/j.tice.2024.102643

Jinan Liu , Jiran Wang , Rui Huang , Xueting Jia , Xiaofeng Huang

Tooth eruption, a critical stage in tooth development, is related to osteoclastogenesis. Intraperitoneal injection of Shh agonists into neonatal mice promoted tooth eruption at postnatal day (PN) 15, whereas treatment with the Shh inhibitor (LDE225) suppressed this process. When RAW264.7 osteoclast precursor cells were treated with RANKL, NFATc1 translocated from the cytoplasm to the nucleus and induced cell differentiation into TRAP⁺ osteoclasts; this process was activated by Shh but inhibited by LDE225. Treating RAW264.7 cells with the p38 inhibitor, BIRB796, also inhibited NFATc1 nuclear localization. p-p38 expression in the alveolar bone of PN3 and PN5 mice was decreased by treatment with LDE225, and RAW264.7 cell differentiation was reduced by BIRB796, regardless of treatment with Shh. Furthermore, Shh activated p38 signaling pathway in RAW264.7 cells, while p38 phosphorylation was reduced by LDE225, which ultimately inhibited osteoclast precursor differentiation. Therefore, we concluded that Shh promotes osteoclast precursor differentiation via the p38-NFATc1 signaling pathway.

{"title":"The Shh-p38-NFATc1 signaling pathway is essential for osteoclastogenesis during tooth eruption","authors":"Jinan Liu , Jiran Wang , Rui Huang , Xueting Jia , Xiaofeng Huang","doi":"10.1016/j.tice.2024.102643","DOIUrl":"10.1016/j.tice.2024.102643","url":null,"abstract":"<div><div>Tooth eruption, a critical stage in tooth development, is related to osteoclastogenesis. Intraperitoneal injection of Shh agonists into neonatal mice promoted tooth eruption at postnatal day (PN) 15, whereas treatment with the Shh inhibitor (LDE225) suppressed this process. When RAW264.7 osteoclast precursor cells were treated with RANKL, NFATc1 translocated from the cytoplasm to the nucleus and induced cell differentiation into TRAP<sup>+</sup> osteoclasts; this process was activated by Shh but inhibited by LDE225. Treating RAW264.7 cells with the p38 inhibitor, BIRB796, also inhibited NFATc1 nuclear localization. p-p38 expression in the alveolar bone of PN3 and PN5 mice was decreased by treatment with LDE225, and RAW264.7 cell differentiation was reduced by BIRB796, regardless of treatment with Shh. Furthermore, Shh activated p38 signaling pathway in RAW264.7 cells, while p38 phosphorylation was reduced by LDE225, which ultimately inhibited osteoclast precursor differentiation. Therefore, we concluded that Shh promotes osteoclast precursor differentiation via the p38-NFATc1 signaling pathway.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"92 ","pages":"Article 102643"},"PeriodicalIF":2.7,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Matrigel-encapsulated articular cartilage derived fibronectin adhesion assay derived chondroprogenitors for enhanced chondrogenic differentiation: An in vitro evaluation

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-26 DOI: 10.1016/j.tice.2024.102638

Ganesh Parasuraman , Mariya Sneha Rani J , Merin Mary Zachariah , Abel Livingston , Elizabeth Vinod

Purpose

In cartilage research, three-dimensional (3D) culture models are pivotal for assessing chondrogenic differentiation potential. Standard pellet cultures, despite their utility, pose challenges like uneven differentiation and handling difficulties. This study explores the use of Matrigel, an extracellular matrix-based hydrogel, to encapsulate fibronectin adhesion assay-derived chondroprogenitors (FAA-CPs) and evaluate their chondrogenic differentiation potential.

Methods

FAA-CPs, isolated from human articular cartilage and expanded to passage 2, were either polymerized in Matrigel or cultured as standard pellets. Both groups underwent chondrogenic differentiation for 28 days and osteogenic differentiation for 21 days. Comprehensive analyses included histological staining, gene expression (SOX-9, ACAN, COL2A1 for chondrogenesis; COL1A1, RUNX2, COL10A1 for osteogenesis), and biochemical assays for glycosaminoglycans (GAG) and Collagen type II.

Results

The results demonstrated that Matrigel-encapsulated FAA-CPs achieved greater GAG accumulation, as evidenced by enhanced Alcian Blue and Safranin O staining, compared to standard pellets. However, the Collagen type II deposition, both histologically and quantitatively, was reduced in Matrigel constructs. Gene expression analysis showed no significant differences in key chondrogenic and osteogenic markers between the two groups. Despite improved handling and GAG deposition, Matrigel did not enhance uniform chondrogenic differentiation nor offer significant benefits for osteogenic differentiation, showing comparable hypertrophic markers to the standard method.

Conclusion

While Matrigel encapsulation offers advantages in handling and enhances GAG accumulation quantitatively, these benefits were not reflected in staining results. Furthermore, Matrigel did not significantly outperform standard pellet cultures in chondrogenic or osteogenic differentiation. These findings suggest a need for further refinement and in vivo validation.

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引用次数: 0

Chondroitin sulfate alleviated lipopolysaccharide-induced arthritis in feline and canine articular chondrocytes through regulation of neurotrophic signaling pathways and apoptosis 硫酸软骨素通过调节神经营养信号通路和细胞凋亡缓解脂多糖诱导的猫科动物和犬科动物关节软骨细胞关节炎

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-26 DOI: 10.1016/j.tice.2024.102642

Huasong Bai , Tong Liu , Hengyan Wang , Yunliang Li , Zhanzhong Wang

Osteoarthritis (OA) is a pervasive degenerative joint disease affecting companion animals, characterized by chronic inflammation and cartilage degradation. However, the effectiveness of chondroitin sulfate (CS) in treating OA in dogs and cats remains controversial. This study aimed to determine the therapeutic effects and molecular mechanisms of CS on lipopolysaccharide (LPS)-induced inflammation in feline and canine articular chondrocytes (FAC and CAC) at the cellular level in vitro. Our findings demonstrated that CS treatment (800 µg/mL) significantly enhanced cell viability and reduced oxidative stress in FAC and CAC, as evidenced by decreased levels of reactive oxygen species and increased activities of antioxidant enzymes. Furthermore, CS treatment effectively suppressed LPS-induced secretion of pro-inflammatory cytokines, including interleukin-1, tumor necrosis factor-α, interleukin-8, interleukin-10, and matrix metalloproteinases-3, and reduced apoptosis, as confirmed by fluorescence staining and flow cytometry. Transcriptomic analysis revealed that CS upregulated neurotrophic signaling pathways, promoting cell survival and proliferation. Metabolomic analysis indicated that CS treatment upregulated metabolites associated with glycerophospholipid and purine metabolism, suggesting enhanced membrane integrity and energy metabolism. Conversely, pathways involved in protein catabolism and arachidonic acid metabolism were downregulated, indicating a reduction in inflammatory mediators. Collectively, these findings elucidate the multifaceted role of CS in modulating chondrocyte metabolism and inflammatory responses, highlighting its potential to alleviate OA.

骨关节炎（OA）是一种影响伴侣动物的普遍性退行性关节疾病，其特点是慢性炎症和软骨退化。然而，硫酸软骨素（CS）治疗猫狗骨关节炎的效果仍存在争议。本研究旨在确定 CS 在体外细胞水平对脂多糖（LPS）诱导的猫科动物和犬科动物关节软骨细胞（FAC 和 CAC）炎症的治疗效果和分子机制。我们的研究结果表明，CS 处理（800 µg/mL）可显著提高 FAC 和 CAC 的细胞活力并降低氧化应激，这体现在活性氧水平的降低和抗氧化酶活性的提高上。此外，经荧光染色和流式细胞术证实，CS 能有效抑制 LPS 诱导的促炎细胞因子（包括白细胞介素-1、肿瘤坏死因子-α、白细胞介素-8、白细胞介素-10 和基质金属蛋白酶-3）的分泌，并减少细胞凋亡。转录组分析表明，CS 上调了神经营养信号通路，促进了细胞的存活和增殖。代谢组分析表明，CS 处理上调了与甘油磷脂和嘌呤代谢相关的代谢物，表明膜完整性和能量代谢得到了增强。相反，参与蛋白质分解代谢和花生四烯酸代谢的途径则出现下调，表明炎症介质减少。总之，这些研究结果阐明了 CS 在调节软骨细胞代谢和炎症反应中的多方面作用，凸显了其缓解 OA 的潜力。

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引用次数: 0

PDE4B abrogation extenuates angiotensin II-induced endothelial dysfunction related to hypertension through up-regulation of AMPK/Sirt1/Nrf2/ARE signaling 通过上调AMPK/Sirt1/Nrf2/ARE信号，消减PDE4B可减轻血管紧张素II诱导的与高血压有关的内皮功能障碍

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-23 DOI: 10.1016/j.tice.2024.102637

Yong Chen, Suipeng Li, Xuqing Hou, Yinfeng Jia

Endothelial dysfunction is commonly perceived as a precursor in the process of hypertension, a severe cardiovascular disorder. Phosphodiesterase 4B (PDE4B) inactivation has been proposed to exert cardioprotective effects and prevent pulmonary hypertension. However, the role of PDE4B in endothelial dysfunction in hypertension remains inexplicit, which will be investigated in the present work. In angiotensin II (Ang II)-induced human umbilical vein endothelial cells (HUVECs), RT-qPCR and Western blotting were used to analyze PDE4B expression. CCK-8 method was used to detect cell viability. Flow cytometry assay and Caspase 3 assay kit were used to detect cellular apoptotic level. Wound healing and tube formation assays were respectively used to detect cell migration and angiogenesis. Western blotting and corresponding assay kits were respectively used to analyze the expressions and contents of endothelial dysfunction markers. JC-1 assay, RT-qPCR and relevant assay kit were respectively used to detect mitochondrial membrane potential (ΔΨm), quantify mitochondrial DNA (mtDNA) copy number and mitochondrial permeability transition pore (mPTP) opening. Besides, Western blotting was used to analyze the expressions of endoplasmic reticulum stress (ERS) and AMP-activated protein kinase (AMPK)/sirtuin 1 (Sirt1)/nuclear factor-erythroid 2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling-associated proteins. PDE4B expression was increased in Ang II- induced HUVECs. PDE4B knockdown promoted the viability, migration, angiogenesis while inhibiting the apoptosis, endothelial dysfunction, ERS and mitochondrial damage in Ang II-induced HUVECs. Additionally, PDE4B silence activated AMPK/Sirt1/Nrf2/ARE pathway and AMPK inhibitor Compound C (CC) partially reversed the effects of PDE4B down-regulation on Ang II-induced HUVECs. Conclusively, PDE4B inhibition might protect against Ang II-induced endothelial dysfunction in HUVECs via up-regulating AMPK/Sirt1/Nrf2/ARE pathway, which might be mediated by the suppression of ERS and mitochondrial damage.

内皮功能障碍通常被认为是高血压这一严重心血管疾病的前兆。磷酸二酯酶 4B (PDE4B) 失活被认为具有保护心脏和预防肺动脉高压的作用。然而，PDE4B 在高血压内皮功能障碍中的作用尚不明确，本研究将对此进行研究。在血管紧张素 II（Ang II）诱导的人脐静脉内皮细胞（HUVECs）中，采用 RT-qPCR 和 Western 印迹法分析 PDE4B 的表达。采用 CCK-8 法检测细胞活力。流式细胞术检测和 Caspase 3 检测试剂盒用于检测细胞凋亡水平。伤口愈合和管形成试验分别用于检测细胞迁移和血管生成。Western 印迹法和相应的检测试剂盒分别用于分析内皮功能障碍标志物的表达和含量。JC-1检测、RT-qPCR和相关检测试剂盒分别用于检测线粒体膜电位（ΔΨm）、线粒体DNA（mtDNA）拷贝数定量和线粒体通透性转换孔（mPTP）开放。此外，还采用 Western 印迹法分析了内质网应激（ERS）和 AMPK 激活蛋白激酶（AMPK）/sirtuin 1（Sirt1）/核因子红细胞 2 相关因子 2（Nrf2）/抗氧化反应元件（ARE）信号相关蛋白的表达。在 Ang II 诱导的 HUVECs 中，PDE4B 的表达增加。PDE4B 敲除可促进 Ang II 诱导的 HUVECs 的活力、迁移和血管生成，同时抑制其凋亡、内皮功能障碍、ERS 和线粒体损伤。此外，PDE4B 沉默激活了 AMPK/Sirt1/Nrf2/ARE 通路，AMPK 抑制剂化合物 C（CC）部分逆转了 PDE4B 下调对 Ang II 诱导的 HUVECs 的影响。结论是，PDE4B抑制可通过上调AMPK/Sirt1/Nrf2/ARE通路保护HUVECs免受Ang II诱导的内皮功能障碍，而AMPK/Sirt1/Nrf2/ARE通路可能是通过抑制ERS和线粒体损伤介导的。

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引用次数: 0

Pharmacotherapeutic potential of pratensein to avert metribuzin instigated hepatotoxicity via regulating TGF-β1, PI3K/Akt, Nrf-2/Keap-1 and NF-κB pathway 普拉滕辛通过调节 TGF-β1、PI3K/Akt、Nrf-2/Keap-1 和 NF-κB 通路，具有避免甲ribuzin 引起的肝毒性的药疗潜力

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-22 DOI: 10.1016/j.tice.2024.102635

Hesham M. Hassan , Mahmoud El Safadi , Warda Mustfa , Shahaba Tehreem , Giorgio Antoniolli , Arifa Mehreen , Adnan Ali , Ahmed Al-Emam

Metribuzin (MBN) is a selective herbicide that adversely damages the vital organs of the body including the liver. Pratensein (PTN) is a novel flavonoid that exhibits marvelous medicinal properties. This experimental trial commenced to elucidate the pharmacotherapeutic strength of PTN to counteract MBN provoked liver toxicity in rats. Thirty-six male albino rats (Rattus norvegicus) were categorized into four groups i.e., the control, MBN (133.33 mg/kg), MBN (133.33 mg/kg) + PTN (20 mg/kg) and PTN (20 mg/kg) alone treated group. Our findings revealed that MBN exposure promoted the expressions of Keap-1 as well as concentrations of ROS and MDA while reducing the gene expressions of Nrf-2 as well as activities of catalase (CAT), glutathione Peroxidase (GPx), glutathione reductase (GSR), heme oxygenase-1 (HO-1), superoxide dismutase (SOD) and glutathione (GSH) contents. The levels of albumin and total proteins were reduced whereas the levels of alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were enhanced following the MBN administration. Moreover, the gene expression of transforming growth Factor–β1 (TGF-β1), matrix metallopeptidase-2 (MMP-2), matrix metallopeptidase-9 (MMP-9), collagen, type I, alpha 1 and type-3 alpha were escalated in response to MBN intoxication. Furthermore, MBN administration cause a sudden upregulation in the levels of NF-κB, IL-1β, TNF-α, IL-6 & COX-2. Besides, MBN exposure enhanced the gene expression of Bax and Caspase-3 while reducing the gene expression of PI3K, Akt and Bcl-2. Additionally, MBN exposure dysregulated the normal histology of liver. However, PTN treatment notably protected the hepatic tissues via regulating abovementioned dysregulations due to its marvelous ROS scavenging potential.

灭草津（MBN）是一种选择性除草剂，会对包括肝脏在内的人体重要器官造成不利损害。Pratensein（PTN）是一种新型黄酮类化合物，具有神奇的药用功效。本实验旨在阐明PTN在对抗甲基溴对大鼠肝脏毒性方面的药理作用。36 只雄性白化大鼠（Rattus norvegicus）被分为四组，即对照组、MBN（133.33 毫克/千克）组、MBN（133.33 毫克/千克）+ PTN（20 毫克/千克）组和单用 PTN（20 毫克/千克）组。我们的研究结果表明，MBN 暴露促进了 Keap-1 的表达以及 ROS 和 MDA 的浓度，同时降低了 Nrf-2 的基因表达以及过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GPx)、谷胱甘肽还原酶 (GSR)、血红素加氧酶-1 (HO-1)、超氧化物歧化酶 (SOD) 和谷胱甘肽 (GSH) 的含量。服用 MBN 后，白蛋白和总蛋白水平降低，而碱性磷酸酶（ALP）、γ-谷氨酰转移酶（GGT）、天冬氨酸氨基转移酶（AST）和丙氨酸氨基转移酶（ALT）水平升高。此外，转化生长因子-β1（TGF-β1）、基质金属肽酶-2（MMP-2）、基质金属肽酶-9（MMP-9）、胶原蛋白、Ⅰ型、α1 和α-3 型的基因表达也随甲基溴中毒而增加。此外，甲基溴的施用导致 NF-κB、IL-1β、TNF-α、IL-6 和 COX-2 水平突然上调。此外，暴露于 MBN 会增强 Bax 和 Caspase-3 的基因表达，同时降低 PI3K、Akt 和 Bcl-2 的基因表达。此外，暴露于 MBN 会导致肝脏正常组织学失调。然而，由于 PTN 具有出色的清除 ROS 的潜力，它能通过调节上述失调来保护肝组织。

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引用次数: 0

SIRT7 promotes dental pulp stem cells replicative senescence through desuccinylation of ROCK1

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-22 DOI: 10.1016/j.tice.2024.102636

Rui Zhang , Jie Chen , Yuanyuan Chen , Yangyang Li

The therapeutic effectiveness of dental pulp stem cells (DPSCs) is limited. Sirtuin 7 (SIRT7) has been reported to be associated with a variety of age-related diseases. We aimed to identify the regulatory role of SIRT7 in DPSC senescence and investigate the underlying mechanism. DPSCs were isolated from healthy adults, the stem markers were verified by flow cytomerty analysis. Replicative senescence was induced in DPSCs by serial passage and cells were analyzed at PD16 and 54. DPSC senescence was evaluated by observing senescence-associated β-galactosidase (SA-β-gal) and telomerase reverse transcriptase (TERT) activity. Meanwhile, the markers of senescence levels were monitored by western blotting assay. SIRT7 protein was pulled-down, and the binding relationship between SIRT7 and ROCK1 was verified by immunoprecipitation and western blotting methods. Replicative senescence was induced in DPSCs at PD54. The number of SA-β-gal stained DPSCs significantly increased in the PD54 group while the level of TERT activity was decreased. The cyclin-dependent kinase inhibitors p53, p21, and p16, which are markers of senescence, were markedly up-regulated at PD54. SIRT7 was also found to be lowly expressed at PD54. Inhibition of SIRT7 significantly accelerated the senescence of DPSCs. Moreover, SIRT7 can bind with ROCK1, and SIRT7 could lead to ROCK1 desuccinylation at K520. Inhibited ROCK1 significantly reversed the effects of SIRT7 knockdown on regulating DPSCs senescence. Our results demonstrate that the SIRT7/ROCK1 axis plays a key role in the regulation of DPSC senescence and provide a candidate target to improve the functional and therapeutic potential of DPSCs.

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引用次数: 0

The effects of short-term non-weightbearing and immobilization after anterior cruciate ligament reconstruction on articular cartilage: Long-term observation after reloading and remobilization

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-11-22 DOI: 10.1016/j.tice.2024.102628

Akinori Kaneguchi, Ryo Okahara, Nanami Masuhara, Yoshika Doi, Kaoru Yamaoka, Junya Ozawa

Non-weightbearing or immobilization after anterior cruciate ligament (ACL) reconstruction accelerates cartilage degeneration. However, it is unclear whether these adverse effects are reversed by reloading or remobilization. Moreover, it is unknown whether the combination of non-weightbearing and immobilization after ACL reconstruction has synergistic effects on cartilage degeneration. We aimed to determine 1) the long-term effects of reloading or remobilization following short-term non-weightbearing or immobilization after ACL reconstruction on cartilage degeneration and 2) the combined effects of non-weightbearing and immobilization on cartilage degeneration. We divided ACL-reconstructed rats into four groups: no intervention, non-weightbearing, joint immobilization, and non-weightbearing plus immobilization. Non-weightbearing and immobilization were performed for 2 weeks, after which all rats were reared without intervention. Untreated rats were used as controls. At 2, 4, or 12 weeks after starting the experiment, cartilage degeneration in the anterior, middle, and posterior regions of the medial tibial plateau was histologically assessed. Two weeks of non-weightbearing or immobilization after ACL reconstruction facilitated cartilage degeneration in the middle and posterior regions compared to those with no intervention. Cartilage degeneration was not reversed by 10 weeks of reloading or remobilization. Compared with non-weightbearing alone, combination of non-weightbearing and immobilization improved cartilage degeneration in the middle region, but worsened it in the posterior region. Cartilage degeneration induced by 2 weeks of non-weightbearing or immobilization after ACL reconstruction was not reversed by reloading or remobilization. Thus, to reduce cartilage degeneration, non-weightbearing and immobilization should be avoided after ACL reconstruction, even for short-term.

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引用次数: 0