Cell Proliferation最新文献

{"title":"FAM20C Modulates Neuronal Differentiation in Hypoxic-Ischemic Brain Damage via KAP1 Phosphorylation and LINE1 RNA m6A-Dependent H3K9me3 Regulation.","authors":"Chen-Xi Feng, Mei Wang, Gen Li, Si-Jia Chu, Di Wu, Xiao-Han Hu, Li-Xiao Xu, Mei Li, Xing Feng","doi":"10.1111/cpr.70073","DOIUrl":"https://doi.org/10.1111/cpr.70073","url":null,"abstract":"<p><p>Neurodevelopmental impairment due to hypoxic-ischemic brain damage (HIBD) lacks effective biomarkers and therapeutic targets. Based on some cues from published papers, extracellular serine/threonine protein kinase FAM20C was speculated to play a crucial role in the neurodevelopmental impairment of HIBD. In this study, FAM20C was found suppressed in the ischemic hippocampal tissue of HIBD. The inhibition of FAM20C caused by HIBD affected cell differentiation and subsequently caused cognitive impairment. KAP1 was identified as a kinase substrate of FAM20C in the central nervous system. The regulation of the YTHDC1-NCL-KAP1-LINE1 RNA complex by FAM20C was mediated through KAP1 phosphorylation and LINE1 RNA m6A. These alterations consequently modulated the establishment of the H3K9me3 modification on LINE1 DNA, thereby resulting in neuronal differentiation. Furthermore, E2F4, identified as a transcription factor, regulated FAM20C in HIBD. This research has clarified the novel association between FAM20C and HIBD, laying the foundation for innovative diagnostic and therapeutic strategies to counteract neurodevelopmental disruptions arising from neonatal hypoxic-ischemic encephalopathy (HIE).</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70073"},"PeriodicalIF":5.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of EC-EXOs-Derived THBS3 Targeting CD47 to Regulate BMSCs Differentiation to Ameliorate Bone Loss.","authors":"Jiaojiao Wang, Zhaokai Zhou, Wenjie Chen, Yun Chen, Qiyue Zheng, Yajun Chen, Zhengxiao Ouyang, Ran Xu, Qiong Lu","doi":"10.1111/cpr.70066","DOIUrl":"https://doi.org/10.1111/cpr.70066","url":null,"abstract":"<p><p>With the continuous increase of the elderly population and the deepening of population ageing in China, osteoporosis has gradually become one of the significant public health problems. Elucidating the pathophysiological mechanisms that induce osteoporosis and identifying more effective therapeutic targets is of great clinical significance. In this study, in vitro experiments demonstrated that endothelial cell exosomes (EC-EXOs) promoted osteogenic and inhibited adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Aged and ovariectomy (OVX)-induced osteoporosis mice models injected with EC-EXOs confirmed that EC-EXOs delayed bone loss. Proteomic analysis revealed a key protein regulating the differentiation of BMSCs. Expression of THBS3 was significantly higher in EC-EXOs than in Human microvascular endothelial cells (HMEC-1). In vitro and in vivo experiments further validated that THBS3 promoted BMSCs' osteogenic differentiation, inhibited their adipogenic differentiation, and retarded bone loss. Computational biology analysis found that CD47 is a downstream target and potentially functional receptor in BMSCs that bind to THBS3. THBS3 treatment of BMSCs down-regulated the expression of CD47 in in vitro experiments. The aged/OVX models further confirmed that EC-EXOs can regulate the differentiation of BMSCs and delay the process of bone loss via the THBS3-CD47 axis. CD47 antibody may be a potential therapeutic agent for treating ageing-associated bone loss.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70066"},"PeriodicalIF":5.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan Suppresses FTH1-Driven Ferritinophagy, a Key Correlate of Prognosis in Hepatocellular Carcinoma.","authors":"Xinxiang Cheng, Xin Ge, Chi Zhang, Xingye Yang, Zhengxin Yu, Min Zhang, Wen Cao, Qingtao Ni, Yang Liu, Songbing He, Yin Yuan","doi":"10.1111/cpr.70074","DOIUrl":"https://doi.org/10.1111/cpr.70074","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic options. Ferritinophagy, an autophagy-dependent process regulating iron metabolism, has emerged as a key contributor to ferroptosis and tumour progression. This study hypothesised that the ferritinophagy-related gene FTH1 drives HCC pathogenesis by modulating tryptophan metabolism and reactive oxygen species (ROS)-dependent ferroptosis. To test this, we first analysed TCGA data to identify prognostic ferritinophagy genes, revealing FTH1 as a critical risk factor. Functional experiments using FTH1-knockdown/-overexpressing HCC cell lines and xenograft models demonstrated that FTH1 enhances proliferation, migration, and tumour growth by upregulating CYP1A1/CYP1A2 in the tryptophan pathway, thereby increasing the synthesis of 6-hydroxymelatonin (6-HMT). Mechanistically, 6-HMT suppressed ROS and ferroptosis by inhibiting cytochrome P450 oxidoreductase (POR). Concurrently, intracellular tryptophan levels were found to inhibit NCOA4-mediated selective autophagy of FTH1, stabilising FTH1 levels and promoting tumour survival. Collectively, our findings establish FTH1 as a central regulator of ferritinophagy in HCC and reveal its dual role in linking tryptophan metabolism to redox homeostasis. This result provides a hint of how FTH1 influences HCC pathogenesis and positions the tryptophan metabolism pathway as a promising therapeutic target.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70074"},"PeriodicalIF":5.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.","authors":"Li-Ying Zhang, Yue-Yue Wang, Ri Wen, Tie-Ning Zhang, Ni Yang","doi":"10.1111/cpr.70077","DOIUrl":"https://doi.org/10.1111/cpr.70077","url":null,"abstract":"<p><p>Histone deacetylase(HDAC) is Zn²⁺-dependent histone deacetylases that regulate the key signalling pathways involved in gene transcription. 11 isoforms have been identified. Recent in vitro and in vivo studies have shown that HDACs are involved in the pathophysiology of cardiovascular diseases (CVDs) and play important roles in cell proliferation, differentiation and mitochondrial metabolism. In terms of physiological mechanisms, HDAC1-6 may play important roles in normal cardiac development and physiological function, while HDAC7 regulates angiogenesis. In pathological processes, class I HDACs function as pro-hypertrophic mediators, whereas class II HDACs act as anti-hypertrophic mediators. HDAC1-3, 6, 9, and 11 participate in lipid cell formation, oxidative stress and endothelial cell injury through multiple signalling pathways, contributing to the pathogenesis of atherosclerosis. In addition, HDACs also play a role in CVDs such as heart failure, myocardial fibrosis, pulmonary hypertension and diabetic cardiomyopathy. In view of this, we reviewed the regulatory pathways and molecular targets of HDACs in the pathogenesis of CVD. In addition, we summarise the current discovery of inhibitors targeting HDACs. HDAC inhibitors have shown promising therapeutic progress in animal experiments, but clinical trials to demonstrate their efficacy in humans are still lacking. A better understanding of the role of HDACs in CVD provides a new direction for the development of therapeutic interventions and holds significant research value.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70077"},"PeriodicalIF":5.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF219 RING Finger Domain Mutants Drive Phase Separation to Encapsulate CCR4-NOT and Promote Cell Proliferation.","authors":"Chen Chen, Chenghao Guo, Ke Fang, Chengqi Lin, Zhuojuan Luo","doi":"10.1111/cpr.70072","DOIUrl":"https://doi.org/10.1111/cpr.70072","url":null,"abstract":"<p><p>RING finger protein 219 (RNF219) is a co-factor for the CCR4-NOT deadenylase complex in mammals. Here, we found that mutations within the C3HC4 scaffold of the RING finger domain in RNF219 are capable of forming condensates via liquid-liquid phase separation (LLPS), though the wild-type RING finger domain intrinsically suppresses LLPS. We further demonstrated that the adjacent coiled-coil 1 (CC1) domain promotes the potential of RNF219 to form condensates. Moreover, the mutant RNF219 condensates are able to encapsulate the CCR4-NOT complex, inhibiting the RNA deadenylation activity of CCR4-NOT. Additionally, we observed that RNF219 mutations could promote cell proliferation. These findings suggest a pathogenic mechanism whereby RNF219 mutations could induce CCR4-NOT condensate formation, inhibit deadenylation-dependent mRNA decay and drive cell proliferation.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70072"},"PeriodicalIF":5.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Herbal Medicine for Colorectal Cancer Treatment: Molecular Mechanisms and Clinical Applications.","authors":"Zuqing Su, Yanlin Li, Zihao Zhou, Bing Feng, Haiming Chen, Guangjuan Zheng","doi":"10.1111/cpr.70065","DOIUrl":"https://doi.org/10.1111/cpr.70065","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common malignant tumours and is the second leading cause of cancer-related mortality worldwide. Despite the availability of preventative, diagnostic and treatment methods including endoscopic treatment, surgical intervention, radiotherapy, biologics, salvage therapy and immunotherapy, the mortality rate associated with CRC remains alarming. Consequently, there is a pressing need to search for medicines for the treatment of CRC. Phytomedicines have been shown to suppress the proliferation and metastasis of CRC through various mechanisms, including immune regulation, modulation of gut microbiota, targeting of stem cells, macrophage polarisation, glycolysis, ferroptosis induction, modulation of extracellular vesicles, activation of mitochondria-induced apoptosis, inflammation reduction, oxidative stress management and intervention of autophagy. Furthermore, numerous studies have reported the anti-cancer and anti-metastatic effects of various phytomedicines, including curcumin, resveratrol, berberine, shikonin, dihydroartemisinin, fucoidan, luteolin, andrographolide, piperine, kaempferol, emodin, cannabidiol, tanshinone IIA and evodiamine. In this review, we sort out the effects and mechanisms of phytomedicines on CRC and outline the major phytomedicines commonly used in CRC treatment. We hope that these phytomedicines may serve as promising drugs or important lead compounds for the management of CRC.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70065"},"PeriodicalIF":5.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage Efferocytosis as a Therapeutic Strategy in Intervertebral Disc Degeneration.","authors":"Shijie Chen, Haijun Zhang, Zhaoheng Wang, Daxue Zhu, Yanhu Li, Yizhi Zhang, Dongxin Wang, Shuwei Chen, Huan Liu, Xuewen Kang","doi":"10.1111/cpr.70068","DOIUrl":"https://doi.org/10.1111/cpr.70068","url":null,"abstract":"<p><p>In recent years, a growing number of studies have disclosed the substantial role of macrophages-key immune cells-in the pathological process of intervertebral disc degeneration. Researchers have categorised macrophage phenotypes into M1 and M2 polarisation, associating these polarisations with intervertebral disc degeneration. Essentially, macrophage phenotypes can be classified as either pro-inflammatory or anti-inflammatory. Induced by diverse factors, these distinct polarisation states exert contrary effects on disc injury and repair. Although numerous studies focus on the polarisation of macrophages and the cytokines they secrete in relation to intervertebral disc degeneration, these studies frequently neglect the relationship between the efferocytosis of macrophages and the progression of intervertebral disc degeneration. Efferocytosis is a specialised procedure in which phagocytes, such as macrophages, engulf and eliminate apoptotic cells. This process is crucial for maintaining tissue homeostasis and resolving inflammation. By effectively clearing these dying cells, efferocytosis helps prevent the release of potentially detrimental cellular contents, thereby facilitating healing and the resolution of inflammation. Simultaneously, macrophages digest the engulfed cell debris and release various cytokines that participate in tissue self-repair. Therefore, this article presents an overview of the molecular mechanisms connecting macrophages and their efferocytosis activity to intervertebral disc degeneration, explores new directions for the utilisation of macrophages in the treatment of intervertebral disc degeneration, and discusses the future prospects for the development of therapeutic targets.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70068"},"PeriodicalIF":5.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural Organoids Protect Engineered Heart Tissues From Glucolipotoxicity by Transferring Versican in a Co-Culture System.","authors":"Baochen Bai, Jiting Li, Ze Wang, Yuhan Yang, Jieqing He, Gonglie Chen, Yufan Zhang, Yan Qi, Zhongjun Wan, Lin Cai, Run Wang, Kai Wang, Dongyu Zhao, Jingzhong Zhang, Weihua Huang, Ronald X Xu, Mingzhai Sun, Xiao Han, Yan Liu, Donghui Zhang, Wanying Zhu, Jian Liu, Yuxuan Guo","doi":"10.1111/cpr.70070","DOIUrl":"https://doi.org/10.1111/cpr.70070","url":null,"abstract":"<p><p>Metabolic disorders could cause dysregulated glucose and lipid at the systemic level, but how inter-tissue/organ communications contribute to glucolipotoxicity is difficult to dissect in animal models. To solve this problem, myocardium and nerve tissues were modelled by 3D engineered heart tissues (EHTs) and neural organoids (NOs), which were co-cultured in a generalised medium with normal or elevated glucose/fatty acid contents. Morphology, gene expression, cell death and functional assessments detected no apparent alterations of EHTs and NOs in co-culture under normal conditions. By contrast, NOs significantly ameliorated glucolipotoxicity in EHTs. Transcriptomic and protein secretion assays identified the extracellular matrix protein versican as a key molecule that was transferred from NOs into EHTs in the high-glucose/fatty acid condition. Recombinant versican protein treatment was sufficient to reduce glucolipotoxicity in EHTs. Adeno-associated virus-delivered versican overexpression was sufficient to ameliorate cardiac dysfunction in a murine model of diabetic cardiomyopathy. These data provide the proof-of-concept evidence that inter-tissue/organ communications exist in the co-culture of engineered tissues and organoids, which could be systemically studied to explore potential pathological mechanisms and therapeutic strategies for multi-organ diseases in vitro.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70070"},"PeriodicalIF":5.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Neuroprotective Role of Ginsenoside Rg1 Against Cerebral Ischemia-Reperfusion Damage Through Inhibition of Mitophagy via Blocking Mitophagosome-Lysosome Fusion.","authors":"Lin Ai, Hangui Ren, Yuan Wang, Mengfan Liu, Yufei Qiu, Jiling Feng, Rongchen Dai, Wang Fu, Yongpeng Wang, Zhichao Xi, Hongxi Xu, Feng Wang","doi":"10.1111/cpr.70071","DOIUrl":"https://doi.org/10.1111/cpr.70071","url":null,"abstract":"<p><p>Ginsenoside Rg1 has shown promise in ameliorating cerebral ischemia-reperfusion injury (CIRI). However, its precise molecular mechanisms remain unclear. In this study, an in vitro CIRI model was established using SH-SY5Y and SK-N-AS neuronal cell lines subjected to oxygen-glucose deprivation followed by reoxygenation (OGD/R). For the in vivo model, C57BL/6J mice underwent middle cerebral artery occlusion and subsequent reperfusion (MCAO/R). The protective effects of Rg1 against OGD/R injury were analysed using the CCK-8 assay and the PI exclusion method. The in vivo neuroprotective effects of Rg1 against CIRI were evaluated using various assessments, including brain blood flow, neurological deficits, behavioural tests, TTC, H&E, Nissl and TUNEL staining. Mitophagy was assessed by detecting mitophagy-initiating proteins via Western blotting, transmission electron microscopy, immunohistochemistry and immunofluorescence staining. Additionally, mitochondrial function was assessed by ATP measurement, the JC-1 assay and MitoSOX-based flow cytometry. Our results show that Rg1 significantly mitigated cell death caused by OGD/R and substantially enhanced cell viability in vitro. Moreover, Rg1 alleviated OGD/R-induced mitochondrial dysfunction, as indicated by preserved mitochondrial membrane potential and decreased mitochondrial ROS levels. Mitophagy was induced after OGD treatment, which was subsequently inhibited by Rg1 during reperfusion. Mechanistically, Rg1 disrupted the fusion of mitophagosomes with lysosomes rather than inhibiting mitophagy initiation, leading to an accumulation of mitochondrial proteins and mitophagy-initiating proteins. Notably, prolonged inhibition of mitophagy by Rg1 did not induce cytotoxicity or exacerbate mitochondrial dysfunction. Furthermore, administration of Rg1 in MCAO/R mice significantly improved brain blood reperfusion, reduced infarct volume, improved neurological deficits, preserved brain tissue integrity and decreased neuronal apoptosis. Consistent with the in vitro observations, Rg1 upregulated mitophagy-related protein expression in MCAO/R mouse brain tissues, indicating potential inhibition of mitophagy. In conclusion, our study reveals that Rg1 significantly alleviates CIRI at least partially by suppressing mitophagy, specifically by impeding the fusion of mitophagosomes with lysosomes.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70071"},"PeriodicalIF":5.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanotransduction Mediated by PDLIM5: The Critical Role of Serpin E2/Integrin β3-Cytoskeleton-Nucleoskeleton Axis in Mechanical Osteogenic Programming.","authors":"Yuchao Yang, Shutong Wu, Yining Wang, Jiajun Tang, Jiaxuan Liu, Jinyang Wang, Yunfeng Li, Asmat Ullah Khan, Muhammad Akram Khan, Wenqing Liu, Jinhui Zhu, Konghe Hu, Jingxing Dai, Jun Ouyang","doi":"10.1111/cpr.70067","DOIUrl":"https://doi.org/10.1111/cpr.70067","url":null,"abstract":"<p><p>Despite the regenerative and self-repair capabilities of bone tissues, significant bone loss can result in substantial bone defects. This study was aimed at investigating the role and underlying mechanisms of the mechanosensitive protein PDZ and LIM Domain 5 (PDLIM5) in the osteogenic differentiation of human adipose-derived stem cells (hASCs) under cyclic tensile stress conditions relevant to bone tissue repair. Utilising proteomics and single-cell RNA sequencing, we identified PDLIM5 and serpin E2 as key genes associated with the osteogenic differentiation of stem cells. To evaluate the expression levels of these genes and related proteins, we utilised western blotting, immunofluorescence and alkaline phosphatase (ALP) staining. Furthermore, lentiviral transfection, Cell Counting Kit-8 (CCK-8) assays, transwell migration assays, wound healing assays and protein-protein interaction analyses were conducted to evaluate changes in osteogenic differentiation under both chemical and physical stimuli, as well as to explore the relationship between serine protease inhibitor E2 (serpin E2) and its downstream effector, PDLIM5. The interactions among serpin E2, integrin β3 and PDLIM5 were confirmed through Haematoxylin and Eosin (H&E) staining, immunohistochemistry and immunofluorescence staining of bone tissues and primary adipose-derived stem cells isolated from integrin β3 knockout mice. Our findings indicate that PDLIM5 modulates the osteogenic differentiation of hASCs via a signalling pathway involving serpin E2, integrin β3 and lamin A.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70067"},"PeriodicalIF":5.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}