Cell Proliferation最新文献_第9页

SLC30A4-AS1 Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via the Alternative Splicing of TP53BP1 SLC30A4-AS1 通过 TP53BP1 的替代剪接介导炎症环境中牙周韧带干细胞的衰老

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-21 DOI: 10.1111/cpr.13778

Mei Xu, Dian Gan, Xi-Yu Zhang, Xiao-Tao He, Rui Xin Wu, Yuan Yin, Rui Jin, Lin Li, Yu-Jie Tan, Fa-Ming Chen, Xuan Li, Bei-Min Tian

{"title":"SLC30A4-AS1 Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via the Alternative Splicing of TP53BP1","authors":"Mei Xu, Dian Gan, Xi-Yu Zhang, Xiao-Tao He, Rui Xin Wu, Yuan Yin, Rui Jin, Lin Li, Yu-Jie Tan, Fa-Ming Chen, Xuan Li, Bei-Min Tian","doi":"10.1111/cpr.13778","DOIUrl":"10.1111/cpr.13778","url":null,"abstract":"Periodontal ligament stem cells (PDLSCs) are key cells that suppress periodontal damage during both the progression and recovery stages of periodontitis. Although substantial evidence has demonstrated that incubation under an inflammatory condition may accelerate senescence of PDLSCs, whether cellular senescence in response to inflammatory incubation contributes to cell dysfunction remain unexplored. In this study, we first observed inflammation-caused PDLSC senescence in periodontitis based on comparisons of matched patients, and this cellular senescence was demonstrated in healthy cells that were subjected to inflammatory conditions. We subsequently designed further experiments to investigate the possible mechanism underlying inflammation-induced PDLSC senescence with a particular focus on the role of long noncoding RNAs (lncRNAs). LncRNA microarray analysis and functional gain/loss studies revealed SLC30A4-AS1 as a regulator of inflammation-mediated PDLSC senescence. By full-length transcriptome sequencing, we found that SLC30A4-AS1 interacted with SRSF3 to affect the alternative splicing (AS) of TP53BP1 and alter the expression of TP53BP1-204. Further functional studies showed that decreased expression of TP53BP1-204 reversed PDLSC senescence, and SLC30A4-AS1 overexpression-induced PDLSC senescence was abolished by TP53BP1-204 knockdown. Our data suggest for the first time that SLC30A4-AS1 plays a key role in regulating PDLSC senescence in inflammatory environments by modulating the AS of TP53BP1.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13778","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Targeting Hsp90α to inhibit HMGB1-mediated renal inflammation and fibrosis 靶向 Hsp90α 抑制 HMGB1 介导的肾脏炎症和纤维化。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-20 DOI: 10.1111/cpr.13774

Huizhi Wei, Jinhong Ren, Xiue Feng, Chengxiao Zhao, Yuanlin Zhang, Hongxia Yuan, Fan Yang, Qingshan Li

{"title":"Targeting Hsp90α to inhibit HMGB1-mediated renal inflammation and fibrosis","authors":"Huizhi Wei, Jinhong Ren, Xiue Feng, Chengxiao Zhao, Yuanlin Zhang, Hongxia Yuan, Fan Yang, Qingshan Li","doi":"10.1111/cpr.13774","DOIUrl":"10.1111/cpr.13774","url":null,"abstract":"Renal fibrosis, a terminal manifestation of chronic kidney disease, is characterized by uncontrolled inflammatory responses, increased oxidative stress, tubular cell death, and imbalanced deposition of extracellular matrix. 5,2′-Dibromo-2,4′,5′-trihydroxydiphenylmethanone (LM49), a polyphenol derivative synthesized by our group with excellent anti-inflammatory pharmacological properties, has been identified as a small-molecule inducer of extracellular matrix degradation. Nonetheless, the protective effects and mechanisms of LM49 on renal fibrosis remain unknown. Here, we report LM49 could effectively alleviate renal fibrosis and improve filtration function. Furthermore, LM49 significantly inhibited macrophage infiltration, pro-inflammatory cytokine production and oxidative stress. Interestingly, in HK-2 cells induced by tumour necrosis factor alpha under oxygen–glucose-serum deprivation conditions, LM49 treatment similarly yielded a reduced inflammatory response, elevated cellular viability and suppressed cell necrosis and epithelial-to-mesenchymal transition. Notably, LM49 prominently suppressed the high-mobility group box 1 (HMGB1) expression, nucleocytoplasmic translocation and activation. Mechanistically, drug affinity responsive target stability and cellular thermal shift assay confirmed that LM49 could interact with the target heat shock protein 90 alpha family class A member 1 (Hsp90α), disrupting the direct binding of Hsp90α to HMGB1 and inhibiting the nuclear export of HMGB1, thereby suppressing the inflammatory response, cell necrosis and fibrogenesis. Furthermore, molecular docking and molecular dynamic simulation revealed that LM49 occupied the N-terminal ATP pocket of Hsp90α. Collectively, our findings show that LM49 treatment can ameliorate renal fibrosis through inhibition of HMGB1-mediated inflammation and necrosis via binding to Hsp90α, providing strong evidence for its anti-inflammatory and anti-fibrotic actions.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 3","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13774","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Direct reprogramming of fibroblasts into spiral ganglion neurons by defined transcription factors 通过定义转录因子将成纤维细胞直接重编程为螺旋神经节神经元。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-17 DOI: 10.1111/cpr.13775

Yuhang Huang, Zhen Chen, Jiang Chen, Jingyue Liu, Cui Qiu, Qing Liu, Linqing Zhang, Guang-Jie Zhu, Xiaofeng Ma, Shuohao Sun, Yun Stone Shi, Guoqiang Wan

引用次数: 0

The apoptotic and anti-proliferative effects of Neosetophomone B in T-cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition Neosetophomone B 通过抑制 PI3K/AKT/mTOR 通路对 T 细胞急性淋巴细胞白血病具有凋亡和抗增殖作用。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-14 DOI: 10.1111/cpr.13773

Shilpa Kuttikrishnan, Abdul W. Ansari, Muhammad Suleman, Fareed Ahmad, Kirti S. Prabhu, Tamam El-Elimat, Feras Q. Alali, Ammira S. Al Shabeeb Akil, Ajaz A. Bhat, Maysaloun Merhi, Said Dermime, Martin Steinhoff, Shahab Uddin

{"title":"The apoptotic and anti-proliferative effects of Neosetophomone B in T-cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition","authors":"Shilpa Kuttikrishnan, Abdul W. Ansari, Muhammad Suleman, Fareed Ahmad, Kirti S. Prabhu, Tamam El-Elimat, Feras Q. Alali, Ammira S. Al Shabeeb Akil, Ajaz A. Bhat, Maysaloun Merhi, Said Dermime, Martin Steinhoff, Shahab Uddin","doi":"10.1111/cpr.13773","DOIUrl":"10.1111/cpr.13773","url":null,"abstract":"The phosphatidylinositol 3-kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling pathway is pivotal in various cancers, including T-cell acute lymphoblastic leukaemia (T-ALL), a particularly aggressive type of leukaemia. This study investigates the effects of Neosetophomone B (NSP-B), a meroterpenoid fungal metabolite, on T-ALL cell lines, focusing on its anti-cancer mechanisms and therapeutic potential. NSP-B significantly inhibited the proliferation of T-ALL cells by inducing G0/G1 cell cycle arrest and promoting caspase-dependent apoptosis. Additionally, NSP-B led to the dephosphorylation and subsequent inactivation of the PI3K/AKT/mTOR signalling pathway, a critical pathway in cell survival and growth. Molecular docking studies revealed a strong binding affinity of NSP-B to the active site of AKT, primarily involving key residues crucial for its activity. Interestingly, NSP-B treatment also induced apoptosis and significantly reduced proliferation in phytohemagglutinin-activated primary human CD3+ T cells, accompanied by a G0/G1 cell cycle arrest. Importantly, NSP-B did not affect normal primary T cells, indicating a degree of selectivity in its action, targeting only T-ALL cells and activated T cells. In conclusion, our findings highlight the potential of NSP-B as a novel therapeutic agent for T-ALL, specifically targeting the aberrantly activated PI3K/AKT/mTOR pathway and being selective in action. These results provide a strong basis for further investigation into NSP-B's anti-cancer properties and potential application in T-ALL clinical therapies.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 3","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13773","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Synergy between pluripotent stem cell-derived macrophages and self-renewing macrophages: Envisioning a promising avenue for the modelling and cell therapy of infectious diseases 多能干细胞衍生巨噬细胞与自我更新巨噬细胞之间的协同作用：为传染性疾病的建模和细胞治疗开辟一条前景广阔的道路。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-13 DOI: 10.1111/cpr.13770

Dingkun Peng, Meilin Li, Zhuoran Yu, Tingsheng Yan, Meng Yao, Su Li, Zhonghua Liu, Lian-Feng Li, Hua-Ji Qiu

{"title":"Synergy between pluripotent stem cell-derived macrophages and self-renewing macrophages: Envisioning a promising avenue for the modelling and cell therapy of infectious diseases","authors":"Dingkun Peng, Meilin Li, Zhuoran Yu, Tingsheng Yan, Meng Yao, Su Li, Zhonghua Liu, Lian-Feng Li, Hua-Ji Qiu","doi":"10.1111/cpr.13770","DOIUrl":"10.1111/cpr.13770","url":null,"abstract":"As crucial phagocytes of the innate immune system, macrophages (Mϕs) protect mammalian hosts, maintain tissue homeostasis and influence disease pathogenesis. Nonetheless, Mϕs are susceptible to various pathogens, including bacteria, viruses and parasites, which cause various infectious diseases, necessitating a deeper understanding of pathogen–Mϕ interactions and therapeutic insights. Pluripotent stem cells (PSCs) have been efficiently differentiated into PSC-derived Mϕs (PSCdMϕs) resembling primary Mϕs, advancing the modelling and cell therapy of infectious diseases. However, the mass production of PSCdMϕs, which lack proliferative capacity, relies on large-scale expansions of PSCs, thereby increasing both costs and culture cycles. Notably, Mϕs deficient in the MafB/c-Maf genes have been reported to re-enter the cell cycle with the stimulation of specific growth factor cocktails, turning into self-renewing Mϕs (SRMϕs). This review summarizes the applications of PSCdMϕs in the modelling and cell therapy of infectious diseases and strategies for establishing SRMϕs. Most importantly, we innovatively propose that PSCs can serve as a gene editing platform to creating PSC-derived SRMϕs (termed PSRMϕs), addressing the resistance of Mϕs against genetic manipulation. We discuss the challenges and possible solutions in creating PSRMϕs. In conclusion, this review provides novel insights into the development of physiologically relevant and expandable Mϕ models, highlighting the enormous potential of PSRMϕs as a promising avenue for the modelling and cell therapy of infectious diseases.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 2","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13770","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Predicting tumour resistance to paclitaxel and carboplatin utilising genome-wide screening in haploid human embryonic stem cells 利用单倍体人类胚胎干细胞的全基因组筛选预测肿瘤对紫杉醇和卡铂的耐药性。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-10 DOI: 10.1111/cpr.13771

Jonathan Nissenbaum, Emanuel Segal, Hagit Philip, Rivki Cashman, Tamar Golan-Lev, Benjamin E. Reubinoff, Adi Turjeman, Ofra Yanuka, Elyad Lezmi, Oded Kopper, Nissim Benvenisty

{"title":"Predicting tumour resistance to paclitaxel and carboplatin utilising genome-wide screening in haploid human embryonic stem cells","authors":"Jonathan Nissenbaum, Emanuel Segal, Hagit Philip, Rivki Cashman, Tamar Golan-Lev, Benjamin E. Reubinoff, Adi Turjeman, Ofra Yanuka, Elyad Lezmi, Oded Kopper, Nissim Benvenisty","doi":"10.1111/cpr.13771","DOIUrl":"10.1111/cpr.13771","url":null,"abstract":"Taxanes and platinum molecules, specifically paclitaxel and carboplatin, are widely used anticancer drugs that induce cell death and serve as first-line chemotherapy for various cancer types. Despite the efficient effect of both drugs on cancer cell proliferation, many tumours have innate resistance against paclitaxel and carboplatin, which leads to inefficient treatment and poor survival rates. Haploid human embryonic stem cells (hESCs) are a novel and robust platform for genetic screening. To gain a comprehensive view of genes that affect or regulate paclitaxel and carboplatin resistance, genome-wide loss-of-function screens in haploid hESCs were performed. Both paclitaxel and carboplatin screens have yielded selected plausible gene lists and pathways relevant to resistance prediction. The effects of mutations in selected genes on the resistance to the drugs were demonstrated. Based on the results, an algorithm that can predict resistance to paclitaxel or carboplatin was developed. Applying the algorithm to the DNA mutation profile of patients' tumours enabled the separation of sensitive versus resistant patients, thus, providing a prediction tool. As the anticancer drugs arsenal can offer alternatives in case of resistance to either paclitaxel or carboplatin, an early prediction can provide a significant advantage and should improve treatment. The algorithm assists this unmet need and helps predict whether a patient will respond to the treatment and may have an immediate clinically actionable application.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 3","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13771","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Featured Cover 精选封面

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-11-04 DOI: 10.1111/cpr.13769

Yuwen Luo, Jun Li, Lv Zheng, Yizaitiguli Reyimjan, Yan Ma, Shuaixiang Huang, Hongyu Liu, Guizhen Zhou, Jiachen Bai, Yixiao Zhu, Yidan Sun, Xinhua Zou, Yunpeng Hou, Xiangwei Fu

引用次数: 0

Crotonylation of MCM6 enhances chemotherapeutics sensitivity of breast cancer via inducing DNA replication stress MCM6 的巴豆酰化可通过诱导 DNA 复制应激提高乳腺癌的化疗敏感性。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-30 DOI: 10.1111/cpr.13759

Haoyun Song, Zhao Guo, Kun Xie, Xiangwen Liu, Xuguang Yang, Rong Shen, Degui Wang

{"title":"Crotonylation of MCM6 enhances chemotherapeutics sensitivity of breast cancer via inducing DNA replication stress","authors":"Haoyun Song, Zhao Guo, Kun Xie, Xiangwen Liu, Xuguang Yang, Rong Shen, Degui Wang","doi":"10.1111/cpr.13759","DOIUrl":"10.1111/cpr.13759","url":null,"abstract":"Breast cancer is associated with high morbidity and mortality, which are closely influenced by protein post-translational modifications (PTMs). Lysine crotonylation (Kcr) serves as a newly identified PTM type that plays a role in various biological processes; however, its involvement in breast cancer progression remains unclear. Minichromosome maintenance 6 (MCM6) is a critical component of DNA replication and has been previous confirmed to exhibit a significant role in tumorigenesis. Despite this, a comprehensive analysis of MCM6, particularly regarding its modifications in breast cancer is lacking. In this study, we found MCM6 is upregulated in breast invasive carcinoma (BRCA) and is associated with poorer overall survival by regulating the DNA damage repair mechanisms. Furthermore, MCM6-knockdown resulted in decreased cell proliferation and inhibited the DNA replication, leading to DNA replication stress and sustained DNA damage, thereby enhancing the chemotherapeutic sensitivity of breast cancer. Additionally, SIRT7-mediated crotonylation of MCM6 at K599 (MCM6-K599cr) was significantly upregulated in response to DNA replication stress, primarily due to the disassemebly of the MCM2-7 complex and regulated by RNF8-mediated ubiquitination. Concurrently, kaempferol, which acts as a regulator of SIRT7, was found to enhance the Kcr level of MCM6, reducing tumour weight, particular when combined with paclitaxel, highlighting its potential chemotherapeutic target for BRCA therapy.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 2","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13759","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

RETRACTION: Tanshinone I attenuates the malignant biological properties of ovarian cancer by inducing apoptosis and autophagy via the inactivation of PI3K/AKT/mTOR pathway 返回：丹参酮 I 通过使 PI3K/AKT/mTOR 通路失活，诱导细胞凋亡和自噬，从而减轻卵巢癌的恶性生物学特性。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-23 DOI: 10.1111/cpr.13768

{"title":"RETRACTION: Tanshinone I attenuates the malignant biological properties of ovarian cancer by inducing apoptosis and autophagy via the inactivation of PI3K/AKT/mTOR pathway","authors":"","doi":"10.1111/cpr.13768","DOIUrl":"10.1111/cpr.13768","url":null,"abstract":"\u0000 J. Zhou, Y.-y. Jiang, H. Chen, Y.-c. Wu, and L. Zhang, “ Tanshinone I Attenuates the Malignant Biological Properties of Ovarian Cancer by Inducing Apoptosis and Autophagy via the Inactivation of PI3K/AKT/mTOR Pathway,” Cell Proliferation 53, no. 2 (2020): e12739. https://doi.org/10.1111/cpr.12739.The above article, published online on 09 December 2019, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Deputy Editor, Yunfeng Lin; and John Wiley & Sons Ltd. A third party contacted the publisher to report that duplicated images had been detected in multiple different articles by different author groups, each of which described different experimental conditions. The image duplications are listed as follows: Images in Figure 1C were duplicated in Wang et al. 2019 (https://doi.org/10.2147/OTT.S221161), which was submitted and published prior to the publication of this article in Cell Proliferation. In addition, duplicate images from Figures 1C, 1D, 2C, 3B, 3D, 4C, 4D, and 5D were detected in many other articles by different author groups that had been published subsequent to this article.The authors responded to an inquiry by the publisher regarding these concerns and shared what were labeled as original images for Figures 1–6 but did not share the original images for the cell proliferation assays that had been used in Figure 1. The editors reviewed this evidence and found that it did not properly explain the duplications across different articles. The retraction has been agreed to because the duplications of images across different articles fundamentally compromises the conclusions and results presented in the article. The authors disagree with the retraction.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 2","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13768","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy 单核转录组学揭示了肩袖撕裂诱发肌肉萎缩后的退行性肌核亚群。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-22 DOI: 10.1111/cpr.13763

Ziying Sun, Xi Cheng, Zheng Wang, Chenfeng Qiao, Hong Qian, Tao Yuan, Zhongyang Lv, Wenshuang Sun, Hanwen Zhang, Yuan Liu, Zhihao Lu, Jintao Lin, Chengteng Lai, Yang Wang, Xiaojiang Yang, Xingyun Wang, Jia Meng, Nirong Bao

{"title":"Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy","authors":"Ziying Sun, Xi Cheng, Zheng Wang, Chenfeng Qiao, Hong Qian, Tao Yuan, Zhongyang Lv, Wenshuang Sun, Hanwen Zhang, Yuan Liu, Zhihao Lu, Jintao Lin, Chengteng Lai, Yang Wang, Xiaojiang Yang, Xingyun Wang, Jia Meng, Nirong Bao","doi":"10.1111/cpr.13763","DOIUrl":"10.1111/cpr.13763","url":null,"abstract":"Rotator cuff tear (RCT) is the primary cause of shoulder pain and disability and frequently trigger muscle degeneration characterised by muscle atrophy, fatty infiltration and fibrosis. Single-nucleus RNA sequencing (snRNA-seq) was used to reveal the transcriptional changes in the supraspinatus muscle after RCT. Supraspinatus muscles were obtained from patients with habitual shoulder dislocation (n = 3) and RCT (n = 3). In response to the RCT, trajectory analysis showed progression from normal myonuclei to ANKRD1+ myonuclei, which captured atrophy-and fatty infiltration-related regulons (KLF5, KLF10, FOSL1 and BHLHE40). Transcriptomic alterations in fibro/adipogenic progenitors (FAPs) and muscle satellite cells (MuSCs) have also been studied. By predicting cell–cell interactions, we observed communication alterations between myofibers and muscle-resident cells following RCT. Our findings reveal the plasticity of muscle cells in response to RCT and offer valuable insights into the molecular mechanisms and potential therapeutic targets of RCT.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 3","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13763","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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