STEM CELLS最新文献_第6页

Correction to: Division-Independent Differentiation of Muscle Stem Cells During a Growth Stimulus. 更正：肌肉干细胞在生长刺激过程中的独立分裂分化

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae021

引用次数: 0

Past and future of alveolar organoids for lung regenerative medicine. 肺泡器官组织用于肺再生医学的过去与未来

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae024

Ryuta Mikawa, Shimpei Gotoh

{"title":"Past and future of alveolar organoids for lung regenerative medicine.","authors":"Ryuta Mikawa, Shimpei Gotoh","doi":"10.1093/stmcls/sxae024","DOIUrl":"10.1093/stmcls/sxae024","url":null,"abstract":"The lung is regarded as having limited regenerative capacity, and there are few treatment options for refractory lung diseases, such as interstitial pneumonia. Lung transplantation is the final option available in some scenarios. Research in this area has been slow owing to the complex structure of the lung for efficient gas exchange between the alveolar spaces and capillaries as well as the difficulty in obtaining specimens from patients with progressive lung disease. However, basic research over the past decade in the field of mouse and human embryology using genetic lineage tracing techniques and stem cell biology using primary and pluripotent stem cell-derived alveolar organoids has begun to clarify the tissue response in various intractable lung diseases and the mechanisms underlying remodeling. Advancement in this area may expand potential therapeutic targets for alveolar regeneration, providing alternatives to lung transplantation, and contribute to the development of effective therapeutic methods that activate or repopulate stem cells in the lung. In this review, we cover research focused on alveolar epithelial cells and discuss methods expected to regenerate lungs that are damaged by diseases.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"491-498"},"PeriodicalIF":5.2,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DKK1 Activates the PI3K/AKT Pathway via CKAP4 to Balance the Inhibitory Effect on Wnt/β-Catenin Signaling and Regulates Wnt3a-Induced MSC Migration. DKK1 通过 CKAP4 激活 PI3K/AKT 通路，以平衡对 Wnt/β-catenin 信号的抑制作用，并调节 Wnt3a 诱导的间充质干细胞迁移。

IF 4 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae022

Huanhuan Chen, Ya'nan Hu, Xiaojing Xu, Yan Dai, Hongxiang Qian, Xinyu Yang, Jinming Liu, Qisheng He, Huanxiang Zhang

{"title":"DKK1 Activates the PI3K/AKT Pathway via CKAP4 to Balance the Inhibitory Effect on Wnt/β-Catenin Signaling and Regulates Wnt3a-Induced MSC Migration.","authors":"Huanhuan Chen, Ya'nan Hu, Xiaojing Xu, Yan Dai, Hongxiang Qian, Xinyu Yang, Jinming Liu, Qisheng He, Huanxiang Zhang","doi":"10.1093/stmcls/sxae022","DOIUrl":"10.1093/stmcls/sxae022","url":null,"abstract":"Wnt/β-catenin signaling plays a crucial role in the migration of mesenchymal stem cells (MSCs). However, our study has revealed an intriguing phenomenon where Dickkopf-1 (DKK1), an inhibitor of Wnt/β-catenin signaling, promotes MSC migration at certain concentrations ranging from 25 to 100 ng/mL while inhibiting Wnt3a-induced MSC migration at a higher concentration (400 ng/mL). Interestingly, DKK1 consistently inhibited Wnt3a-induced phosphorylation of LRP6 at all concentrations. We further identified cytoskeleton-associated protein 4 (CKAP4), another DKK1 receptor, to be localized on the cell membrane of MSCs. Overexpressing the CRD2 deletion mutant of DKK1 (ΔCRD2), which selectively binds to CKAP4, promoted the accumulation of active β-catenin (ABC), the phosphorylation of AKT (Ser473) and the migration of MSCs, suggesting that DKK1 may activate Wnt/β-catenin signaling via the CKAP4/PI3K/AKT cascade. We also investigated the effect of the CKAP4 intracellular domain mutant (CKAP4-P/A) that failed to activate the PI3K/AKT pathway and found that CKAP4-P/A suppressed DKK1 (100 ng/mL)-induced AKT activation, ABC accumulation, and MSC migration. Moreover, CKAP4-P/A significantly weakened the inhibitory effects of DKK1 (400 ng/mL) on Wnt3a-induced MSC migration and Wnt/β-catenin signaling. Based on these findings, we propose that DKK1 may activate the PI3K/AKT pathway via CKAP4 to balance the inhibitory effect on Wnt/β-catenin signaling and thus regulate Wnt3a-induced migration of MSCs. Our study reveals a previously unrecognized role of DKK1 in regulating MSC migration, highlighting the importance of CKAP4 and PI3K/AKT pathways in this process.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"567-579"},"PeriodicalIF":4.0,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stem cell dynamics and cellular heterogeneity across lineage subtypes of castrate-resistant prostate cancer. 干细胞动态和阉割耐药前列腺癌不同亚型的细胞异质性。

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae025

Michael L Beshiri, Brian J Capaldo, Ross Lake, Anson T Ku, Danielle Burner, Caitlin M Tice, Crystal Tran, Julianna Kostas, Aian Neil Alilin, JuanJuan Yin, Supreet Agarwal, Samantha A Morris, Fatima H Karzai, Tamara L Lotan, William L Dahut, Adam G Sowalsky, Kathleen Kelly

{"title":"Stem cell dynamics and cellular heterogeneity across lineage subtypes of castrate-resistant prostate cancer.","authors":"Michael L Beshiri, Brian J Capaldo, Ross Lake, Anson T Ku, Danielle Burner, Caitlin M Tice, Crystal Tran, Julianna Kostas, Aian Neil Alilin, JuanJuan Yin, Supreet Agarwal, Samantha A Morris, Fatima H Karzai, Tamara L Lotan, William L Dahut, Adam G Sowalsky, Kathleen Kelly","doi":"10.1093/stmcls/sxae025","DOIUrl":"10.1093/stmcls/sxae025","url":null,"abstract":"To resist lineage-dependent therapies such as androgen receptor inhibition, prostate luminal epithelial adenocarcinoma cells often adopt a stem-like state resulting in lineage plasticity and phenotypic heterogeneity. Castrate-resistant prostate adenocarcinoma can transition to neuroendocrine (NE) and occasionally to amphicrine, co-expressed luminal and NE, phenotypes. We developed castrate-resistant prostate cancer (CRPC) patient-derived organoid models that preserve heterogeneity of the originating tumor, including an amphicrine model displaying a range of luminal and NE phenotypes. To gain biological insight and to identify potential treatment targets within heterogeneous tumor cell populations, we assessed the lineage hierarchy and molecular characteristics of various CRPC tumor subpopulations. Transcriptionally similar stem/progenitor (St/Pr) cells were identified for all lineage populations. Lineage tracing in amphicrine CRPC showed that heterogeneity originated from distinct subclones of infrequent St/Pr cells that produced mainly quiescent differentiated amphicrine progeny. By contrast, adenocarcinoma CRPC progeny originated from St/Pr cells and self-renewing differentiated luminal cells. Neuroendocrine prostate cancer (NEPC) was composed almost exclusively of self-renewing St/Pr cells. Amphicrine subpopulations were enriched for secretory luminal, mesenchymal, and enzalutamide treatment persistent signatures that characterize clinical progression. Finally, the amphicrine St/Pr subpopulation was specifically depleted with an AURKA inhibitor, which blocked tumor growth. These data illuminate distinct stem cell (SC) characteristics for subtype-specific CRPC in addition to demonstrating a context for targeting differentiation-competent prostate SCs.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"526-539"},"PeriodicalIF":5.2,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11177157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Embryonic stem cell related gene regulates alternative splicing of transcription factor 3 to maintain human embryonic stem cells' self-renewal and pluripotency. ESRG 可调控 TCF3 的替代剪接，以维持 hESCs 的自我更新和多能性。

IF 4 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae020

Wen Xie, Weidong Liu, Lei Wang, Shasha Li, Zilin Liao, Hongjuan Xu, Yihan Li, Xingjun Jiang, Caiping Ren

{"title":"Embryonic stem cell related gene regulates alternative splicing of transcription factor 3 to maintain human embryonic stem cells' self-renewal and pluripotency.","authors":"Wen Xie, Weidong Liu, Lei Wang, Shasha Li, Zilin Liao, Hongjuan Xu, Yihan Li, Xingjun Jiang, Caiping Ren","doi":"10.1093/stmcls/sxae020","DOIUrl":"10.1093/stmcls/sxae020","url":null,"abstract":"Exploring the mechanism of self-renewal and pluripotency maintenance of human embryonic stem cells (hESCs) is of great significance in basic research and clinical applications, but it has not been fully elucidated. Long non-coding RNAs (lncRNAs) have been shown to play a key role in the self-renewal and pluripotency maintenance of hESCs. We previously reported that the lncRNA ESRG, which is highly expressed in undifferentiated hESCs, can maintain the self-renewal and pluripotency of hPSCs. RNA pull-down mass spectrometry showed that ESRG could bind to other proteins, among which heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) attracted our attention. In this study, we showed that HNRNPA1 can maintain self-renewal and pluripotency of hESCs. ESRG bound to and stabilized HNRNPA1 protein through the ubiquitin-proteasome pathway. In addition, knockdown of ESRG or HNRNPA1 resulted in alternative splicing of TCF3, which originally and primarily encoded E12, to mainly encode E47 and inhibit CDH1 expression. HNRNPA1 could rescue the biological function changes of hESCs caused by ESRG knockdown or overexpression. Our results suggest that ESRG regulates the alternative splicing of TCF3 to affect CDH1 expression and maintain hESCs self-renewal and pluripotency by binding and stabilizing HNRNPA1 protein. This study lays a good foundation for exploring the new molecular regulatory mechanism by which ESRG maintains hESCs self-renewal and pluripotency.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"540-553"},"PeriodicalIF":4.0,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139929260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Organoid-based personalized medicine: from tumor outcome prediction to autologous transplantation. 基于类器官的个性化医疗：从肿瘤结果预测到自体移植。

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-06-14 DOI: 10.1093/stmcls/sxae023

Abel Soto-Gamez, Jeremy P Gunawan, Lara Barazzuol, Sarah Pringle, Rob P Coppes

{"title":"Organoid-based personalized medicine: from tumor outcome prediction to autologous transplantation.","authors":"Abel Soto-Gamez, Jeremy P Gunawan, Lara Barazzuol, Sarah Pringle, Rob P Coppes","doi":"10.1093/stmcls/sxae023","DOIUrl":"10.1093/stmcls/sxae023","url":null,"abstract":"Inter-individual variation largely influences disease susceptibility, as well as response to therapy. In a clinical context, the optimal treatment of a disease should consider inter-individual variation and formulate tailored decisions at an individual level. In recent years, emerging organoid technologies promise to capture part of an individual's phenotypic variability and prove helpful in providing clinically relevant molecular insights. Organoids are stem cell-derived 3-dimensional models that contain multiple cell types that can self-organize and give rise to complex structures mimicking the organization and functionality of the tissue of origin. Organoids therefore represent a more faithful recapitulation of the dynamics of the tissues of interest, compared to conventional monolayer cultures, thus supporting their use in evaluating disease prognosis, or as a tool to predict treatment outcomes. Additionally, the individualized nature of patient-derived organoids enables the use of autologous organoids as a source of transplantable material not limited by histocompatibility. An increasing amount of preclinical evidence has paved the way for clinical trials exploring the applications of organoid-based technologies, some of which are in phase I/II. This review focuses on the recent progress concerning the use of patient-derived organoids in personalized medicine, including (1) diagnostics and disease prognosis, (2) treatment outcome prediction to guide therapeutic advice, and (3) organoid transplantation or cell-based therapies. We discuss examples of these potential applications and the challenges associated with their future implementation.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"499-508"},"PeriodicalIF":5.2,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11177156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

S-Adenosyl-l-Methionine Alleviates the Senescence of MSCs Through the PI3K/AKT/FOXO3a Signaling Pathway. S-腺苷-L-蛋氨酸通过 PI3K/AKT/FOXO3a 信号通路缓解间充质干细胞的衰老。

IF 4 2区医学

STEM CELLS Pub Date : 2024-05-15 DOI: 10.1093/stmcls/sxae010

Lipeng Shang, Xiaoxia Li, Xiaoyan Ding, Guoxiang Liu, Zhen Pan, Xiangyan Chen, Yuelei Wang, Bing Li, Ting Wang, Robert Chunhua Zhao

{"title":"S-Adenosyl-l-Methionine Alleviates the Senescence of MSCs Through the PI3K/AKT/FOXO3a Signaling Pathway.","authors":"Lipeng Shang, Xiaoxia Li, Xiaoyan Ding, Guoxiang Liu, Zhen Pan, Xiangyan Chen, Yuelei Wang, Bing Li, Ting Wang, Robert Chunhua Zhao","doi":"10.1093/stmcls/sxae010","DOIUrl":"10.1093/stmcls/sxae010","url":null,"abstract":"Cellular senescence significantly affects the proliferative and differentiation capacities of mesenchymal stem cells (MSCs). Identifying key regulators of senescence and exploring potential intervention strategies, including drug-based approaches, are active areas of research. In this context, S-adenosyl-l-methionine (SAM), a critical intermediate in sulfur amino acid metabolism, emerges as a promising candidate for mitigating MSC senescence. In a hydrogen peroxide-induced MSC aging model (100 μM for 2 hours), SAM (50 and 100 μM) was revealed to alleviate the senescence of MSCs, and also attenuated the level of reactive oxygen species and enhanced the adipogenic and osteogenic differentiation in senescent MSCs. In a premature aging mouse model (subcutaneously injected with 150 mg/kg/day d-galactose in the neck and back for 7 weeks), SAM (30 mg/kg/day by gavage for 5 weeks) was shown to delay the overall aging process while increasing the number and thickness of bone trabeculae in the distal femur. Mechanistically, activation of PI3K/AKT signaling and increased phosphorylation of forkhead box O3 (FOXO3a) was proved to be associated with the antisenescence role of SAM. These findings highlight that the PI3K/AKT/FOXO3a axis in MSCs could play a crucial role in MSCs senescence and suggest that SAM may be a potential therapeutic drug for MSCs senescence and related diseases.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"475-490"},"PeriodicalIF":4.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140011787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mesenchymal Stromal/Stem Cells Know Best: The Remarkable Complexities of Its Interactions With Polymorphonuclear Neutrophils. 间充质基质/干细胞（MSCs）最清楚：它与多形核中性粒细胞（PMNs）的相互作用异常复杂。

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-05-15 DOI: 10.1093/stmcls/sxae011

Li-Tzu Wang, Wei Lee, Ko-Jiunn Liu, Huey-Kang Sytwu, Men-Luh Yen, B Linju Yen

{"title":"Mesenchymal Stromal/Stem Cells Know Best: The Remarkable Complexities of Its Interactions With Polymorphonuclear Neutrophils.","authors":"Li-Tzu Wang, Wei Lee, Ko-Jiunn Liu, Huey-Kang Sytwu, Men-Luh Yen, B Linju Yen","doi":"10.1093/stmcls/sxae011","DOIUrl":"10.1093/stmcls/sxae011","url":null,"abstract":"Polymorphonuclear neutrophils (PMNs), the predominant immune cell type in humans, have long been known as first-line effector cells against bacterial infections mainly through phagocytosis and production of reactive oxygen species (ROS). However, recent research has unveiled novel and pivotal roles of these abundant but short-lived granulocytes in health and disease. Human mesenchymal stromal/stem cells (MSCs), renowned for their regenerative properties and modulation of T lymphocytes from effector to regulatory phenotypes, exhibit complex and context-dependent interactions with PMNs. Regardless of species or source, MSCs strongly abrogate PMN apoptosis, a critical determinant of PMN function, except if PMNs are highly stimulated. MSCs also have the capacity to fine-tune PMN activation, particularly in terms of CD11b expression and phagocytosis. Moreover, MSCs can modulate numerous other PMN functions, spanning migration, ROS production, and neutrophil extracellular trap (NET) formation/NETosis, but directionality is remarkably dependent on the underlying context: in normal nondiseased conditions, MSCs enhance PMN migration and ROS production, whereas in inflammatory conditions, MSCs reduce both these functions and NETosis. Furthermore, the state of the MSCs themselves, whether isolated from diseased or healthy donors, and the specific secreted products and molecules, can impact interactions with PMNs; while healthy MSCs prevent PMN infiltration and NETosis, MSCs isolated from patients with cancer promote these functions. This comprehensive analysis highlights the intricate interplay between PMNs and MSCs and its profound relevance in healthy and pathological conditions, shedding light on how to best strategize the use of MSCs in the expanding list of diseases with PMN involvement.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"403-415"},"PeriodicalIF":5.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139680447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HucMSCs Delay Muscle Atrophy After Peripheral Nerve Injury Through Exosomes by Repressing Muscle-Specific Ubiquitin Ligases. HucMSCs 通过外泌体抑制肌肉特异性泛素连接酶，从而延缓周围神经损伤后的肌肉萎缩。

IF 4 2区医学

STEM CELLS Pub Date : 2024-05-15 DOI: 10.1093/stmcls/sxae017

Jian Chen, Yaqiong Zhu, Hui Gao, Xianghui Chen, Dan Yi, MoLin Li, Li Wang, Guanhui Xing, Siming Chen, Jie Tang, Yuexiang Wang

{"title":"HucMSCs Delay Muscle Atrophy After Peripheral Nerve Injury Through Exosomes by Repressing Muscle-Specific Ubiquitin Ligases.","authors":"Jian Chen, Yaqiong Zhu, Hui Gao, Xianghui Chen, Dan Yi, MoLin Li, Li Wang, Guanhui Xing, Siming Chen, Jie Tang, Yuexiang Wang","doi":"10.1093/stmcls/sxae017","DOIUrl":"10.1093/stmcls/sxae017","url":null,"abstract":"Cell therapy based on mesenchymal stem cells (MSCs) alleviate muscle atrophy caused by diabetes and aging; however, the impact of human umbilical cord mesenchymal stem cells on muscle atrophy following nerve injury and the underlying mechanisms remain unclear. In this study, we evaluated the therapeutic efficacy of human umbilical cord MSCs (hucMSCs) and hucMSC-derived exosomes (hucMSC-EXOs) for muscle atrophy following nerve injury and identified the underlying molecular mechanisms. Sciatic nerve crush injury in rats and the induction of myotubes in L6 cells were used to determine the ameliorating effect of hucMSCs and hucMSC-EXOs on muscle atrophy. Q-PCR and Western blot analyses were used to measure the expression of muscle-specific ubiquitin ligases Fbxo32 (Atrogin1, MAFbx) and Trim63 (MuRF-1). Dual-luciferase reporter gene experiments were conducted to validate the direct binding of miRNAs to their target genes. Local injection of hucMSCs and hucMSC-EXOs mitigated atrophy in the rat gastrocnemius muscle following sciatic nerve crush injury. In vitro, hucMSC-EXOs alleviated atrophy in L6 myotubes. Mechanistic analysis indicated the upregulation of miR-23b-3p levels in L6 myotubes following hucMSC-EXOs treatment. MiR-23b-3p significantly inhibited the expression of its target genes, Fbxo32 and Trim63, and suppressed myotube atrophy. Notably, an miR-23b-3p inhibitor reversed the inhibitory effect of miR-23b-3p on myotube atrophy in vitro. These results suggest that hucMSCs and their exosomes alleviate muscle atrophy following nerve injury. MiR-23b-3p in exosomes secreted by hucMSCs contributes to this mechanism by inhibiting the muscle-specific ubiquitination ligases Fbxo32 and Trim63.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"460-474"},"PeriodicalIF":4.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11094387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139929261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Uterine Immunoprivileged Cells Restore Cardiac Function of Male Recipients After Myocardial Infarction. 子宫免疫细胞可恢复心肌梗塞后男性受体的心脏功能。

IF 5.2 2区医学

STEM CELLS Pub Date : 2024-05-15 DOI: 10.1093/stmcls/sxae008

Zexu Peng, Ana Ludke, Jun Wu, Shuhong Li, Faisal J Alibhai, Yichong Zhang, Yunfei Fan, Huifang Song, Sheng He, Jun Xie, Ren-Ke Li

{"title":"Uterine Immunoprivileged Cells Restore Cardiac Function of Male Recipients After Myocardial Infarction.","authors":"Zexu Peng, Ana Ludke, Jun Wu, Shuhong Li, Faisal J Alibhai, Yichong Zhang, Yunfei Fan, Huifang Song, Sheng He, Jun Xie, Ren-Ke Li","doi":"10.1093/stmcls/sxae008","DOIUrl":"10.1093/stmcls/sxae008","url":null,"abstract":"It has been documented that the uterus plays a key cardio-protective role in pre-menopausal women, which is supported by uterine cell therapy, to preserve cardiac functioning post-myocardial infarction, being effective among females. However, whether such therapies would also be beneficial among males is still largely unknown. In this study, we aimed to fill in this gap in knowledge by examining the effects of transplanted uterine cells on infarcted male hearts. We identified, based on major histocompatibility complex class I (MHC-I) expression levels, 3 uterine reparative cell populations: MHC-I(neg), MHC-I(mix), and MHC-I(pos). In vitro, MHC-I(neg) cells showed higher levels of pro-angiogenic, pro-survival, and anti-inflammatory factors, compared to MHC-I(mix) and MHC-I(pos). Furthermore, when cocultured with allogeneic mixed leukocytes, MHC-I(neg) had lower cytotoxicity and leukocyte proliferation. In particular, CD8+ cytotoxic T cells significantly decreased, while CD4+CD25+ Tregs and CD4-CD8- double-negative T cells significantly increased when cocultured with MHC-I(neg), compared to MHC-I(mix) and MHC-I(pos) cocultures. In vivo, MHC-I(neg) as well as MHC-I(mix) were found under both syngeneic and allogeneic transplantation in infarcted male hearts, to significantly improve cardiac function and reduce the scar size, via promoting angiogenesis in the infarcted area. All of these findings thus support the view that males could also benefit from the cardio-protective effects observed among females, via cell therapy approaches involving the transplantation of immuno-privileged uterine reparative cells in infarcted hearts.","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":"430-444"},"PeriodicalIF":5.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139519411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0