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CD34+ stromal cells/telocytes and their role in mouse lung development: Light microscopy, immunofluorescence, ultrastructural and scanning electron microscopy evidence CD34+ 基质细胞/骨髓细胞及其在小鼠肺发育中的作用:光镜、免疫荧光、超微结构和扫描电子显微镜证据。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-08-04 DOI: 10.1002/cbin.12223
Ganesh Dama, Chengxu Xue, Yangxia Zhang, Dezhuang Li, Jinyu Fan, Liang Qiao, Zhihao Xu, Ciqing Yang, Yanli Liu, Mohammad Farris Iman Leong Bin Abdullah, Juntang Lin

Telocytes (TCs), a novel type of mesenchymal or interstitial cell with specific, very long and thin cellular prolongations, have been found in various mammalian organs and have potential biological functions. However, their existence during lung development is poorly understood. This study aimed to investigate the existence, morphological features, and role of CD34+ SCs/TCs in mouse lungs from foetal to postnatal life using primary cell culture, double immunofluorescence, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). The immunofluorescence double staining profiles revealed positive expression of CD34 and PDGFR-α, Sca-1 or VEGFR-3, and the expression of these markers differed among the age groups during lung development. Intriguingly, in the E18.5 stage of development, along with the CD34+ SCs/TCs, haematopoietic stem cells and angiogenic factors were also significantly increased in number compared with those in the E14.5, E16.5, P0 and P7. Subsequently, TEM confirmed that CD34+ SCs/TCs consisted of a small cell body with long telopodes (Tps) that projected from the cytoplasm. Tps consisted of alternating thin and thick segments known as podomers and podoms. TCs contain abundant endoplasmic reticulum, mitochondria and secretory vesicles and establish close connections with neighbouring cells. Furthermore, SEM revealed characteristic features, including triangular, oval, spherical, or fusiform cell bodies with extensive cellular prolongations, depending on the number of Tps. Our findings provide evidence for the existence of CD34+ SCs/TCs, which contribute to vasculogenesis, the formation of the air‒blood barrier, tissue organization during lung development and homoeostasis.

远端细胞(TCs)是一种新型间质细胞或间质细胞,具有特异性的、非常细长的细胞延伸,已在多种哺乳动物器官中发现,并具有潜在的生物学功能。然而,人们对它们在肺发育过程中的存在还知之甚少。本研究旨在采用原代细胞培养、双重免疫荧光、透射电子显微镜(TEM)和扫描电子显微镜(SEM)等方法,研究CD34+ SCs/TCs在小鼠从胎儿到出生后肺部的存在、形态特征和作用。免疫荧光双重染色图谱显示,CD34和PDGFR-α、Sca-1或VEGFR-3呈阳性表达,这些标记物在肺发育过程中的表达在不同年龄组间存在差异。耐人寻味的是,与E14.5、E16.5、P0和P7相比,在E18.5发育阶段,除了CD34+ SCs/TCs,造血干细胞和血管生成因子的数量也显著增加。随后,TEM 证实,CD34+ SCs/TCs 由一个小细胞体和从细胞质中伸出的长端粒(Tps)组成。Tps由被称为podomers和podoms的薄片和厚片交替组成。TC含有丰富的内质网、线粒体和分泌泡,并与邻近细胞建立密切联系。此外,扫描电子显微镜(SEM)显示了一些特征,包括三角形、椭圆形、球形或纺锤形细胞体,这些细胞体具有广泛的细胞延伸,具体取决于 Tps 的数量。我们的研究结果为 CD34+ SCs/TCs 的存在提供了证据,它们有助于血管生成、气血屏障的形成、肺部发育过程中的组织结构和平衡。
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引用次数: 0
DEAD/H-box helicase 11 is transcriptionally activated by Yin Yang-1 and accelerates oral squamous cell carcinoma progression DEAD/H-box螺旋酶11被阴阳-1转录激活,并加速口腔鳞状细胞癌的进展。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-08-01 DOI: 10.1002/cbin.12228
Guang Yang, Xin Shi, Meixia Zhang, Kaiwen Wang, Xin Tian, Xiaofeng Wang

Oral squamous cell carcinoma (OSCC) is the most common oral malignancy. DEAD/H-box helicase 11 (DDX11), a DNA helicase, has been implicated in the progression of several cancers. Yet, the precise function of DDX11 in OSCC is poorly understood. The DDX11 expression in OSCC cells and normal oral keratinocytes was evaluated in the Gene Expression Omnibus database (GSE146483 and GSE31853). SCC-4 and CAL-27 cells expressing doxycycline-inducible DDX11 or DDX11 shRNA were generated by lentiviral infection. The role of DDX11 in OSCC cells was determined by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, colony formation assay, flow cytometry assay, TUNEL staining, and western blot. The effects of DDX11 on tumor growth were explored in a xenograft nude mouse model. The relationship between DDX11 and transcription factor Yin Yang-1 (YY1) was researched using the dual luciferase report assay and chromatin immunoprecipitation assay. DDX11 expression was significantly upregulated in OSCC cells. Knockdown of DDX11 inhibited cell proliferation, induced cell cycle arrest, and suppressed PI3K-AKT pathway, while DDX11 overexpression showed opposite effects. The number of apoptotic cells was increased in DDX11 silenced cells. DDX11 upregulation or knockdown accelerated or suppressed tumor growth in vivo, respectively. Moreover, the YY1 bound and activated the DDX11 promoter, resulting in increasing DDX11 expression. Forced expression DDX11 reversed the anticancer effects of YY1 silencing on OSCC cells. DDX11 has tumor-promoting function in OSCC and is transcriptionally regulated by YY1, indicating that DDX11 may serve as a potential target for the OSCC treatment.

口腔鳞状细胞癌(OSCC)是最常见的口腔恶性肿瘤。DEAD/H-box螺旋酶11(DDX11)是一种DNA螺旋酶,与多种癌症的进展有关联。然而,DDX11在OSCC中的确切功能却鲜为人知。基因表达总库数据库(GSE146483和GSE31853)评估了DDX11在OSCC细胞和正常口腔角质细胞中的表达情况。通过慢病毒感染生成了表达强力霉素诱导型 DDX11 或 DDX11 shRNA 的 SCC-4 和 CAL-27 细胞。通过3-(4, 5-二甲基噻唑-2-基)-2, 5-二苯基溴化四氮唑试验、集落形成试验、流式细胞术试验、TUNEL染色和Western印迹检测了DDX11在OSCC细胞中的作用。在异种移植裸鼠模型中探讨了 DDX11 对肿瘤生长的影响。利用双荧光素酶报告实验和染色质免疫沉淀实验研究了DDX11与转录因子阴阳-1(YY1)之间的关系。DDX11在OSCC细胞中表达明显上调。敲除 DDX11 可抑制细胞增殖、诱导细胞周期停滞并抑制 PI3K-AKT 通路,而 DDX11 的过表达则表现出相反的作用。DDX11沉默的细胞中凋亡细胞数量增加。DDX11 的上调或敲除分别加速或抑制了体内肿瘤的生长。此外,YY1 结合并激活了 DDX11 启动子,导致 DDX11 表达增加。强制表达 DDX11 逆转了 YY1 沉默对 OSCC 细胞的抗癌作用。DDX11在OSCC中具有肿瘤促进功能,并受YY1的转录调控,这表明DDX11可能成为治疗OSCC的潜在靶点。
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引用次数: 0
CRH upregulates supervillin through ERK and AKT pathways to promote bladder cancer cell migration CRH 通过 ERK 和 AKT 途径上调 supervillin,促进膀胱癌细胞迁移。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-08-01 DOI: 10.1002/cbin.12227
Rongchen Mao, Feier Zhou, Yali Hong, Yongqi Li, Chao Zhu, Lai Jin, Shengnan Li

Corticotropin-releasing hormone (CRH) has been well documented playing a role in the regulation of cellular processes, immune responses, and inflammatory processes that can influence the occurrence and development of tumors. Supervillin (SVIL) is a membrane-associated and actin-binding protein, which is actively involved in the proliferation, spread, and migration of cancer cells. This work investigated CRH's influence on bladder cancer cells' migration and relevant mechanisms. By using human bladder cancer cells T24 and RT4 in wound healing experiments and transwell assay, we found that the migration ability of the T24 cells was significantly increased after CRH treatment. In vivo experiments showed that CRH significantly promoted the metastases of T24 cells in cell line-derived xenograft (CDX) mouse model. Interestingly, downregulation of SVIL by SVIL-specifc small hairpin RNAs significantly reduced the promoting effect of CRH on bladder cancer cell migration. Furthermore, CRH significantly increased SVIL messenger RNA and protein expression in T24 cells, accompanied with AKT and ERK phosphorylation in T24 cells. Pretreatment with AKT inhibitor (MK2206) blocked the CRH-induced SVIL expression and ERK phosphorylation. Also, inhibition of ERK signaling pathway by U0126 significantly reduced the CRH-induced SVIL expression and AKT phosphorylation. It suggested that cross-talking between AKT and ERK pathways was involved in the effect of CRH on SVIL. Taken together, we demonstrated that CRH induced migration of bladder cancer cells, in which AKT and ERK pathways -SVIL played a key role.

有大量文件证明,促肾上腺皮质激素释放激素(CRH)在细胞过程、免疫反应和炎症过程的调节中发挥作用,从而影响肿瘤的发生和发展。Supervillin (SVIL) 是一种膜相关的肌动蛋白结合蛋白,积极参与癌细胞的增殖、扩散和迁移。这项研究探讨了CRH对膀胱癌细胞迁移的影响及其相关机制。通过使用人膀胱癌细胞T24和RT4进行伤口愈合实验和透孔实验,我们发现CRH处理后T24细胞的迁移能力明显增强。体内实验表明,在细胞系异种移植(CDX)小鼠模型中,CRH能明显促进T24细胞的转移。有趣的是,通过SVIL-specifc小发夹核糖核酸下调SVIL,可明显降低CRH对膀胱癌细胞迁移的促进作用。此外,CRH能明显增加T24细胞中SVIL信使RNA和蛋白的表达,并伴随T24细胞中AKT和ERK的磷酸化。AKT抑制剂(MK2206)可阻断CRH诱导的SVIL表达和ERK磷酸化。此外,用 U0126 抑制 ERK 信号通路也能显著降低 CRH 诱导的 SVIL 表达和 AKT 磷酸化。这表明AKT和ERK通路之间的交叉作用参与了CRH对SVIL的影响。综上所述,我们证明了CRH诱导膀胱癌细胞迁移,其中AKT和ERK通路-SVIL发挥了关键作用。
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引用次数: 0
Overexpression of EGFL7 promotes angiogenesis and nerve regeneration in peripheral nerve injury 过表达EGFL7可促进周围神经损伤的血管生成和神经再生。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-30 DOI: 10.1002/cbin.12221
Zengtao Hao, Zhiqi Huo, Qicheng Aixin-Jueluo, Tao Wu, Yihong Chen

Peripheral nerve injury (PNI) often leads to significant functional impairment. Here, we investigated the impact of epidermal growth factor-like domain-containing protein 7 (EGFL7) on angiogenesis and nerve regeneration following PNI. Using a sciatic nerve injury model, we assessed nerve function using the sciatic nerve function index. We analyzed the expression levels of EGFL7, forkhead box proteins A1 (FOXA1), nerve growth factor (NGF), brain-derived neurotrophic factors (BDNF), Neurofilament 200 (NF200), myelin protein zero (P0), cell adhesion molecule 1 (CD31), vascular endothelial growth factor (VEGF), and NOTCH-related proteins in tissues and cells. Cell proliferation, migration, and angiogenesis were evaluated through cell counting kit assays, 5-ethynyl-2′deoxyuridine staining, and Transwell assays. We investigated the binding of FOXA1 to the EGFL7 promoter using dual-luciferase assays and chromatin immunoprecipitation. We observed decreased EGFL7 expression and increased FOXA1 expression in PNI, and EGFL7 overexpression alleviated gastrocnemius muscle atrophy, increased muscle weight, and improved motor function. Additionally, EGFL7 overexpression enhanced Schwann cell and endothelial cell proliferation and migration, promoted tube formation, and upregulated NGF, BDNF, NF200, P0, CD31, and VEGF expression. FOXA1 was found to bind to the EGFL7 promoter region, inhibiting EGFL7 expression and activating the NOTCH signaling pathway. Notably, FOXA1 overexpression counteracted the effects of EGFL7 on Schwann cells and endothelial cells. In conclusion, EGFL7 holds promise as a therapeutic molecule for treating sciatic nerve injury.

周围神经损伤(PNI)通常会导致严重的功能障碍。在这里,我们研究了表皮生长因子样结构域含蛋白 7(EGFL7)对周围神经损伤后血管生成和神经再生的影响。我们利用坐骨神经损伤模型,使用坐骨神经功能指数评估神经功能。我们分析了组织和细胞中 EGFL7、叉头盒蛋白 A1 (FOXA1)、神经生长因子 (NGF)、脑源性神经营养因子 (BDNF)、神经丝蛋白 200 (NF200)、髓鞘蛋白 0 (P0)、细胞粘附分子 1 (CD31)、血管内皮生长因子 (VEGF) 和 NOTCH 相关蛋白的表达水平。通过细胞计数试剂盒检测、5-乙炔基-2'脱氧尿苷染色和 Transwell 检测评估了细胞增殖、迁移和血管生成。我们使用双荧光素酶测定法和染色质免疫沉淀法研究了 FOXA1 与 EGFL7 启动子的结合。我们观察到 PNI 中 EGFL7 表达减少,FOXA1 表达增加,EGFL7 的过表达缓解了腓肠肌萎缩,增加了肌肉重量,改善了运动功能。此外,EGFL7 的过表达还能增强许旺细胞和内皮细胞的增殖和迁移,促进管形成,并上调 NGF、BDNF、NF200、P0、CD31 和 VEGF 的表达。研究发现,FOXA1 可与 EGFL7 启动子区域结合,抑制 EGFL7 的表达并激活 NOTCH 信号通路。值得注意的是,FOXA1的过表达抵消了EGFL7对许旺细胞和内皮细胞的影响。总之,EGFL7有望成为治疗坐骨神经损伤的治疗分子。
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引用次数: 0
Tumor-associated macrophages: A sentinel of innate immune system in tumor microenvironment gone haywire 肿瘤相关巨噬细胞:肿瘤微环境失控时先天免疫系统的哨兵
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-25 DOI: 10.1002/cbin.12226
Shaivy Malik, Niti Sureka, Sana Ahuja, Durre Aden, Samreen Zaheer, Sufian Zaheer

The tumor microenvironment (TME) is a critical determinant in the initiation, progression, and treatment outcomes of various cancers. Comprising of cancer-associated fibroblasts (CAF), immune cells, blood vessels, and signaling molecules, the TME is often likened to the soil supporting the seed (tumor). Among its constituents, tumor-associated macrophages (TAMs) play a pivotal role, exhibiting a dual nature as both promoters and inhibitors of tumor growth. This review explores the intricate relationship between TAMs and the TME, emphasizing their diverse functions, from phagocytosis and tissue repair to modulating immune responses. The plasticity of TAMs is highlighted, showcasing their ability to adopt either protumorigenic or anti-tumorigenic phenotypes based on environmental cues. In the context of cancer, TAMs' pro-tumorigenic activities include promoting angiogenesis, inhibiting immune responses, and fostering metastasis. The manuscript delves into therapeutic strategies targeting TAMs, emphasizing the challenges faced in depleting or inhibiting TAMs due to their multifaceted roles. The focus shifts towards reprogramming TAMs to an anti-tumorigenic M1-like phenotype, exploring interventions such as interferons, immune checkpoint inhibitors, and small molecule modulators. Noteworthy advancements include the use of CSF1R inhibitors, CD40 agonists, and CD47 blockade, demonstrating promising results in preclinical and clinical settings. A significant section is dedicated to Chimeric Antigen Receptor (CAR) technology in macrophages (CAR-M cells). While CAR-T cells have shown success in hematological malignancies, their efficacy in solid tumors has been limited. CAR-M cells, engineered to infiltrate solid tumors, are presented as a potential breakthrough, with a focus on their development, challenges, and promising outcomes. The manuscript concludes with the exploration of third-generation CAR-M technology, offering insight into in-vivo reprogramming and nonviral vector approaches. In conclusion, understanding the complex and dynamic role of TAMs in cancer is crucial for developing effective therapeutic strategies. While early-stage TAM-targeted therapies show promise, further extensive research and larger clinical trials are warranted to optimize their targeting and improve overall cancer treatment outcomes.

肿瘤微环境(TME)是决定各种癌症的发生、发展和治疗效果的关键因素。肿瘤微环境由癌症相关成纤维细胞(CAF)、免疫细胞、血管和信号分子组成,通常被比喻为支撑种子(肿瘤)的土壤。在其组成成分中,肿瘤相关巨噬细胞(TAMs)扮演着举足轻重的角色,具有双重性质,既是肿瘤生长的促进因素,也是肿瘤生长的抑制因素。这篇综述探讨了 TAMs 与 TME 之间错综复杂的关系,强调了它们从吞噬和组织修复到调节免疫反应的多种功能。文章强调了TAMs的可塑性,展示了它们根据环境线索采用原致癌表型或抗致癌表型的能力。在癌症方面,TAMs 的促致癌活动包括促进血管生成、抑制免疫反应和促进转移。手稿深入探讨了针对 TAMs 的治疗策略,强调了由于 TAMs 的多方面作用,在消耗或抑制 TAMs 方面所面临的挑战。重点转向将 TAMs 重编程为抗肿瘤的 M1 类表型,探索干扰素、免疫检查点抑制剂和小分子调节剂等干预措施。值得注意的进展包括 CSF1R 抑制剂、CD40 激动剂和 CD47 阻断剂的使用,这些药物在临床前和临床环境中都取得了可喜的成果。有很大一部分内容是关于巨噬细胞(CAR-M 细胞)中的嵌合抗原受体(CAR)技术。虽然 CAR-T 细胞在血液恶性肿瘤中取得了成功,但在实体瘤中的疗效却很有限。本文介绍了可浸润实体瘤的CAR-M细胞,将其作为一项潜在的突破,并重点阐述了其发展、挑战和有望取得的成果。手稿最后探讨了第三代 CAR-M 技术,深入介绍了体内重编程和非病毒载体方法。总之,了解 TAMs 在癌症中复杂而动态的作用对于开发有效的治疗策略至关重要。虽然早期的 TAM 靶向疗法前景看好,但仍需进一步开展广泛研究和更大规模的临床试验,以优化其靶向性并改善整体癌症治疗效果。
{"title":"Tumor-associated macrophages: A sentinel of innate immune system in tumor microenvironment gone haywire","authors":"Shaivy Malik,&nbsp;Niti Sureka,&nbsp;Sana Ahuja,&nbsp;Durre Aden,&nbsp;Samreen Zaheer,&nbsp;Sufian Zaheer","doi":"10.1002/cbin.12226","DOIUrl":"10.1002/cbin.12226","url":null,"abstract":"<p>The tumor microenvironment (TME) is a critical determinant in the initiation, progression, and treatment outcomes of various cancers. Comprising of cancer-associated fibroblasts (CAF), immune cells, blood vessels, and signaling molecules, the TME is often likened to the soil supporting the seed (tumor). Among its constituents, tumor-associated macrophages (TAMs) play a pivotal role, exhibiting a dual nature as both promoters and inhibitors of tumor growth. This review explores the intricate relationship between TAMs and the TME, emphasizing their diverse functions, from phagocytosis and tissue repair to modulating immune responses. The plasticity of TAMs is highlighted, showcasing their ability to adopt either protumorigenic or anti-tumorigenic phenotypes based on environmental cues. In the context of cancer, TAMs' pro-tumorigenic activities include promoting angiogenesis, inhibiting immune responses, and fostering metastasis. The manuscript delves into therapeutic strategies targeting TAMs, emphasizing the challenges faced in depleting or inhibiting TAMs due to their multifaceted roles. The focus shifts towards reprogramming TAMs to an anti-tumorigenic M1-like phenotype, exploring interventions such as interferons, immune checkpoint inhibitors, and small molecule modulators. Noteworthy advancements include the use of CSF1R inhibitors, CD40 agonists, and CD47 blockade, demonstrating promising results in preclinical and clinical settings. A significant section is dedicated to Chimeric Antigen Receptor (CAR) technology in macrophages (CAR-M cells). While CAR-T cells have shown success in hematological malignancies, their efficacy in solid tumors has been limited. CAR-M cells, engineered to infiltrate solid tumors, are presented as a potential breakthrough, with a focus on their development, challenges, and promising outcomes. The manuscript concludes with the exploration of third-generation CAR-M technology, offering insight into in-vivo reprogramming and nonviral vector approaches. In conclusion, understanding the complex and dynamic role of TAMs in cancer is crucial for developing effective therapeutic strategies. While early-stage TAM-targeted therapies show promise, further extensive research and larger clinical trials are warranted to optimize their targeting and improve overall cancer treatment outcomes.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1406-1449"},"PeriodicalIF":3.3,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
AML cell-derived exosomes suppress the activation and cytotoxicity of NK cells in AML via PD-1/PD-L1 pathway AML细胞衍生的外泌体通过PD-1/PD-L1途径抑制AML中NK细胞的激活和细胞毒性。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-19 DOI: 10.1002/cbin.12225
Dandan Wang, Fanchen Zhou, Leiyu He, Xiaohong Wang, Lingrui Song, Haoyu Wang, Shibo Sun, Zhaoming Guo, Kun Ma, Jianqiang Xu, Changhao Cui

Exosomes are bilayer lipid bodies and contain a variety of bioactive molecules such as proteins, lipids, and nucleic acids, and so forth. Exosomes derived from solid tumors may play critical roles in tumor development and immune evasion. However, the underlying effects of tumor-derived exosomes on immune function in modulating intercellular crosstalk within the bone marrow niche during acute myeloid leukemia (AML) development and immune evasion remain largely elusive. In this study, we aimed to explore the role of AML-exos in AML immune evasion. First, we isolated tumor-derived exosomes from AML cells (AML-exos) and revealed the presence of programmed cell death ligand-1 (PD-L1) protein in AML-exos. Next, we demonstrated that AML-exos can directly suppress the activation of natural killer (NK) cells and inhibit the cytotoxicity of NK cells, probably through activating the programmed cell death-1 (PD-1)/PD-L1 pathway. Furthermore, the inhibitory effect of AML-exos on NK cells could be alleviated by either PD-L1 inhibitor or antagonist. In summary, we demonstrated that AML-exos possess a PD-L1-dependent tumor-promoting effect which may contribute to immune tolerance in antitumor therapy, but blocking the PD-1/PD-L1 pathway may alleviate the tumor immunosuppression induced by AML-exos. Our findings in this study may offer a new immunotherapy strategy to cure AML.

外泌体是一种双层脂质体,含有多种生物活性分子,如蛋白质、脂质和核酸等。来自实体瘤的外泌体可能在肿瘤发生和免疫逃避中发挥关键作用。然而,在急性髓性白血病(AML)的发展和免疫逃避过程中,肿瘤衍生的外泌体在调节骨髓龛内细胞间串联的过程中对免疫功能的潜在影响仍然难以捉摸。在本研究中,我们旨在探索 AML 外泌体在 AML 免疫逃避中的作用。首先,我们从急性髓细胞白血病细胞(AML-exos)中分离出了肿瘤衍生外泌体,并在AML-exos中发现了程序性细胞死亡配体-1(PD-L1)蛋白。接下来,我们证明了 AML-exos 可直接抑制自然杀伤(NK)细胞的活化,并抑制 NK 细胞的细胞毒性,这可能是通过激活程序性细胞死亡-1(PD-1)/PD-L1 通路实现的。此外,PD-L1抑制剂或拮抗剂都能减轻AML-exos对NK细胞的抑制作用。总之,我们证明了AML-exos具有依赖于PD-L1的肿瘤促进效应,这可能会导致抗肿瘤治疗中的免疫耐受,但阻断PD-1/PD-L1通路可能会减轻AML-exos诱导的肿瘤免疫抑制。我们在这项研究中的发现可能会为治疗急性髓细胞白血病提供一种新的免疫疗法策略。
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引用次数: 0
Mesenchymal stem/stromal cells alleviate early-stage pulmonary fibrosis in a uPAR-dependent manner 间充质干细胞/基质细胞以 uPAR 依赖性方式缓解早期肺纤维化。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-18 DOI: 10.1002/cbin.12222
Anastasia Yu Efimenko, Anna A. Shmakova, Vladimir S. Popov, Natalia A. Basalova, Maxim A. Vigovskiy, Olga A. Grigorieva, Veronika Yu Sysoeva, Polina S. Klimovich, Nikita R. Khabibullin, Vsevolod A. Tkachuk, Kseniya A. Rubina, Ekaterina V. Semina

Pulmonary fibrosis, a debilitating lung disorder characterised by excessive fibrous tissue accumulation in lung parenchyma, compromises respiratory function leading to a life-threatening respiratory failure. While its origins are multifaceted and poorly understood, the urokinase system, including urokinase-type plasminogen activator (uPA) and its receptor (uPAR), plays a significant role in regulating fibrotic response, extracellular matrix remodelling, and tissue repair. Mesenchymal stem/stromal cells (MSCs) hold promise in regenerative medicine for treating pulmonary fibrosis. Our study aimed to investigate the potential of MSCs to inhibit pulmonary fibrosis as well as the contribution of uPAR expression to this effect. We found that intravenous MSC administration significantly reduced lung fibrosis in the bleomycin-induced pulmonary fibrosis model in mice as revealed by MRI and histological evaluations. Notably, administering the MSCs isolated from adipose tissue of uPAR knockout mice (Plaur-/- MSCs) attenuated lung fibrosis to a lesser extent as compared to WT MSCs. Collagen deposition, a hallmark of fibrosis, was markedly reduced in lungs treated with WT MSCs versus Plaur-/- MSCs. Along with that, endogenous uPA levels were affected differently; after Plaur-/- MSCs were administered, the uPA content was specifically decreased within the blood vessels. Our findings support the potential of MSC treatment in attenuating pulmonary fibrosis. We provide evidence that the observed anti-fibrotic effect depends on uPAR expression in MSCs, suggesting that uPAR might counteract the uPA accumulation in lungs.

肺纤维化是一种使人衰弱的肺部疾病,其特点是肺实质中纤维组织过度积聚,损害呼吸功能,导致呼吸衰竭,危及生命。虽然肺纤维化的起源是多方面的,人们对其了解甚少,但尿激酶系统,包括尿激酶型纤溶酶原激活剂(uPA)及其受体(uPAR),在调节纤维化反应、细胞外基质重塑和组织修复方面发挥着重要作用。间充质干/基质细胞(MSCs)在再生医学中有望治疗肺纤维化。我们的研究旨在探讨间充质干细胞抑制肺纤维化的潜力以及uPAR表达对这一效果的贡献。我们发现,通过核磁共振成像和组织学评估,在博莱霉素诱导的肺纤维化模型中,静脉注射间充质干细胞能明显减轻小鼠的肺纤维化。值得注意的是,与WT间充质干细胞相比,从uPAR基因敲除小鼠脂肪组织中分离出的间充质干细胞(Plaur-/-间充质干细胞)能在较小程度上减轻肺纤维化。在使用 WT 间充质干细胞和 Plaur-/- 间充质干细胞治疗的肺中,纤维化的标志--胶原沉积明显减少。与此同时,内源性uPA水平也受到了不同程度的影响;在使用Plaur-/-间充质干细胞后,血管内的uPA含量明显减少。我们的研究结果支持间充质干细胞治疗在减轻肺纤维化方面的潜力。我们提供的证据表明,所观察到的抗纤维化效应取决于间充质干细胞中uPAR的表达,这表明uPAR可能会抵消uPA在肺中的积累。
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引用次数: 0
Induced expression of AMOT reverses adriamycin resistance in breast cancer cells 诱导表达 AMOT 可逆转乳腺癌细胞对阿霉素的耐药性。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-17 DOI: 10.1002/cbin.12198
Haige Zhang, Yingyi Wang, Ya Gao, Mingming Du, Erhu Pan, Mingliang Sun, Xiaozhi Zhang

Adriamycin (ADR) is widely used against breast cancer, but subsequent resistance always occurs. YAP, a downstream protein of angiomotin (AMOT), importantly contributes to ADR resistance, whereas the mechanism is largely unknown. MCF-7 cells and MDA-MB-231 cells were used to establish ADR-resistant cell. Then, mRNA and protein expressions of AMOT and YAP expressions were determined. After AMOT transfection alone or in combination with YAP, the sensitivity of the cells to ADR were evaluated in vitro by examining cell proliferation, apoptosis, and cell cycle, as well as in vivo by examining tumor growth. Additionally, the expressions of proteins in YAP pathway were determined in AMOT-overexpressing cells. In the ADR-resistant cells, the expression of AMOT was decreased while YAP was increased, respectively, and the nucleus localization of YAP was increased at the same time. After AMOT overexpression, these were inhibited, whereas the cell sensitivity to ADR was enhanced. However, the AMOT-induced changes were significantly suppressed by YAP knockdown. The consistent results in vivo showed that AMOT enhanced the inhibition of ADR on tumor growth, and inhibited YAP signaling, evidenced by decreased levels of YAP, CycD1, and p-ERK. Our data revealed that decreased AMOT contributed to ADR resistance in breast cancer cells, which was importantly negatively mediated YAP. These observations provide a potential therapy against breast cancer with ADR resistance.

阿霉素(ADR)被广泛用于治疗乳腺癌,但随后总会出现耐药性。YAP是Angiomotin(AMOT)的下游蛋白,对ADR耐药有重要作用,但其机制尚不清楚。研究人员利用 MCF-7 细胞和 MDA-MB-231 细胞建立了 ADR 抗性细胞。然后测定 AMOT 的 mRNA 和蛋白表达以及 YAP 的表达。在单独转染 AMOT 或与 YAP 联合转染后,通过检测细胞增殖、凋亡和细胞周期评估了体外细胞对 ADR 的敏感性,并通过检测肿瘤生长评估了体内细胞对 ADR 的敏感性。此外,还测定了过表达 AMOT 的细胞中 YAP 通路蛋白的表达情况。在ADR耐药细胞中,AMOT的表达量减少,而YAP的表达量增加,同时YAP的核定位增加。过表达AMOT后,这些现象受到抑制,而细胞对ADR的敏感性却增强了。然而,YAP敲除后,AMOT诱导的变化被明显抑制。体内的一致结果表明,AMOT增强了ADR对肿瘤生长的抑制作用,并抑制了YAP信号转导,表现为YAP、CycD1和p-ERK水平的降低。我们的数据显示,AMOT的减少导致了乳腺癌细胞对ADR的抗性,而这一抗性主要是由YAP负向介导的。这些观察结果为治疗具有 ADR 抗性的乳腺癌提供了一种潜在疗法。
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引用次数: 0
The migrasome as a developmental learning paradigm in cell biology 迁移体是细胞生物学中的发展学习范例。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-15 DOI: 10.1002/cbin.12220
Yujiao Wang, Zirui Wang, Haoran Cui, Leiliang Zhang

Migrasome is a newly discovered organelle composed of small vesicular structures enclosed in membrane structures. Since its discovery in 2014, migrasome has attracted increasing attention in cell biology due to its critical role in multiple disease processes. Its pivotal role in various disease processes, including cell migration, intercellular communication, removal of damaged mitochondria, embryogenesis localization, immune cell chemotaxis, and virus transmission, underscores its significance in biological systems. With research on migrasome steadily increasing, it becomes a unique resource for undergraduate cell biology education. For deeper understanding of migrasome, we applied a bibliometric approach. Here we conducted a comprehensive analysis of migrasome research by retrieving relevant literature from databases such as Web of Science, Scopus, and PubMed using the keywords “migrasome” or “migrasomes.” Employing CiteSpace software and Prism, we analyzed annual publication trends, identified core authors and institutions, assessed national contributions, examined keywords, and scrutinized highly cited literature related to migrasome research. This study presents a comprehensive overview of migrasome research, elucidating its literature characteristics, key contributors, research hotspots, and emerging trends. By shedding light on the current status and future trajectories of migrasome research, we aim to provide valuable insights for teachers in cell biology education. We propose for the integration of migrasome research into undergraduate curricula to enhance the understanding of cell biology among premedical, medical, and biomedical students, thereby fostering a deeper appreciation for the intricate mechanisms governing cellular behavior and disease processes.

迁移体(Migrasome)是一种新发现的细胞器,由封闭在膜结构中的小囊泡结构组成。自2014年被发现以来,migrasome因其在多种疾病过程中的关键作用而在细胞生物学领域引起了越来越多的关注。它在细胞迁移、细胞间通讯、清除受损线粒体、胚胎发生定位、免疫细胞趋化和病毒传播等多种疾病过程中发挥着关键作用,凸显了其在生物系统中的重要意义。随着对迁移体研究的不断深入,它已成为本科生细胞生物学教育的独特资源。为了加深对迁移体的了解,我们采用了文献计量学方法。在此,我们以 "migrasome "或 "migrasomes "为关键词,从Web of Science、Scopus和PubMed等数据库中检索相关文献,对迁移体研究进行了全面分析。利用CiteSpace软件和Prism,我们分析了年度发表趋势,确定了核心作者和机构,评估了国家贡献,检查了关键词,并仔细研究了与迁移体研究相关的高被引文献。本研究全面概述了迁移体研究,阐明了其文献特点、主要贡献者、研究热点和新兴趋势。通过揭示迁移体研究的现状和未来发展轨迹,我们希望为细胞生物学教育领域的教师提供有价值的见解。我们建议将迁移体研究纳入本科生课程,以增强医学预科生、医学生和生物医学专业学生对细胞生物学的理解,从而加深对细胞行为和疾病过程复杂机制的认识。
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引用次数: 0
Microproteins/micropeptides dysregulation contributes to cancer progression and development: A mechanistic review 微蛋白/微肽失调导致癌症进展和发展:机理综述。
IF 3.3 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2024-07-15 DOI: 10.1002/cbin.12219
Paul Rodrigues, Harun Bangali, Eyhab Ali, M. K. Sharma, Bekhzod Abdullaev, Adnan Taan Alkhafaji, Maha Medha Deorari, Rahman S. Zabibah, Ali Haslany

Microproteins, known as micropeptides, are small protein molecules encoded by short open reading frames. These recently identified molecules have been proven to be an essential part of the human proteome that participates in multiple processes, such as DNA repair, mitochondrial respiration, and regulating different signaling pathways. A growing body of studies has evidenced that microproteins exhibit dysregulated expression levels in various malignancies and contribute to tumor progression. It has been reported that microproteins interact with many proteins, such as enzymes (e.g., adenosine triphosphate synthase) and signal transducers (e.g., c-Jun), and regulate malignant cell metabolism, proliferation, and metastasis. Moreover, microproteins have been found to play a significant role in multidrug resistance in vitro and in vivo by their activity in DNA repair pathways. Considering that, this review intended to summarize the roles of microproteins in different aspects of tumorigenesis with diagnostic and therapeutic perspectives.

微蛋白,又称微肽,是由短开放阅读框编码的小分子蛋白质。这些新近发现的分子已被证明是人类蛋白质组的重要组成部分,参与了 DNA 修复、线粒体呼吸和调节不同信号通路等多个过程。越来越多的研究证明,微蛋白在各种恶性肿瘤中的表达水平失调,并导致肿瘤进展。据报道,微蛋白与许多蛋白质相互作用,如酶(如三磷酸腺苷合成酶)和信号转导因子(如 c-Jun),并调控恶性细胞的新陈代谢、增殖和转移。此外,研究还发现,微蛋白通过在 DNA 修复途径中的活性,在体外和体内的多药耐药性中发挥着重要作用。有鉴于此,本综述旨在从诊断和治疗的角度总结微量蛋白在肿瘤发生的不同方面的作用。
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引用次数: 0
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Cell Biology International
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