Cell Proliferation最新文献_第2页

RETRACTION: MATN1-AS1 promotes glioma progression by functioning as ceRNA of miR-200b/c/429 to regulate CHD1 expression. 返回：MATN1-AS1通过作为miR-200b/c/429的ceRNA来调节CHD1的表达，从而促进胶质瘤的进展。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-20 DOI: 10.1111/cpr.13767

引用次数: 0

Terazosin, a repurposed GPR119 agonist, ameliorates mitophagy and β-cell function in NAFPD by inhibiting MST1-Foxo3a signalling pathway. 特拉唑嗪是一种GPR119激动剂，可通过抑制MST1-Foxo3a信号通路改善NAFPD的有丝分裂和β细胞功能。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-16 DOI: 10.1111/cpr.13764

Chenglei Zhang, Jiarui Li, Lijuan Wang, Jie Ma, Xin Li, Yuanyuan Wu, Yanru Ren, Yanhui Yang, Hui Song, Jianning Li, Yi Yang

{"title":"Terazosin, a repurposed GPR119 agonist, ameliorates mitophagy and β-cell function in NAFPD by inhibiting MST1-Foxo3a signalling pathway.","authors":"Chenglei Zhang, Jiarui Li, Lijuan Wang, Jie Ma, Xin Li, Yuanyuan Wu, Yanru Ren, Yanhui Yang, Hui Song, Jianning Li, Yi Yang","doi":"10.1111/cpr.13764","DOIUrl":"https://doi.org/10.1111/cpr.13764","url":null,"abstract":"GPR119 agonists are being developed to safeguard the function of pancreatic β-cells, especially in the context of non-alcoholic fatty pancreas disease (NAFPD) that is closely associated with β-cell dysfunction. This study aims to employ a drug repurposing strategy to screen GPR119 agonists and explore their potential molecular mechanisms for enhancing β-cell function in the context of NAFPD. MIN6 cells were stimulated with palmitic acid (PA), and a NAFPD model was established in GPR119-/- mice fed with a high-fat diet (HFD). Terazosin, identified through screening, was utilized to assess its impact on enhancing β-cell function via the MST1-Foxo3a pathway and mitophagy. Terazosin selectively activated GPR119, leading to increased cAMP and ATP synthesis, consequently enhancing insulin secretion. Terazosin administration improved high blood glucose, obesity, and impaired pancreatic β-cell function in NAFPD mice. It inhibited the upregulation of MST1-Foxo3a expression in pancreatic tissue and enhanced damaged mitophagy clearance, restoring autophagic flux, and improving mitochondrial quantity and structure in β-cells. Nevertheless, GPR119 deficiency negated the positive impact of terazosin on pancreatic β-cell function in NAFPD mice and abolished its inhibitory effect on the MST1-Foxo3a pathway. Terazosin activates GPR119 on the surface of pancreatic β-cells, enhancing mitophagy and alleviating β-cell dysfunction in the context of NAFPD by suppressing the MST1-Foxo3a signalling pathway. Terazosin could be considered a priority treatment for patients with concomitant NAFPD and hypertension.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13764"},"PeriodicalIF":5.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459114","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}

引用次数: 0

Gdf11 regulates left-right asymmetry development through TGF-β signal. Gdf11通过TGF-β信号调节左右不对称发育

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-15 DOI: 10.1111/cpr.13765

Wantao Yao, Zhaohui Wei, Xinning Tian, Jin Tan, Jingwen Liu

{"title":"Gdf11 regulates left-right asymmetry development through TGF-β signal.","authors":"Wantao Yao, Zhaohui Wei, Xinning Tian, Jin Tan, Jingwen Liu","doi":"10.1111/cpr.13765","DOIUrl":"https://doi.org/10.1111/cpr.13765","url":null,"abstract":"During the embryonic developmental stage in vertebrates, internal organs are arranged along the left-right axis. Disruptions in this process can result in congenital diseases or laterality disorders. The molecular mechanisms of left-right asymmetry in vertebrate development remain largely unclear. Due to its straightforward structure, zebrafish has become a favoured model for studying early laterality events. Here, we demonstrate that growth and development factor 11 (Gdf11) is essential for left-right development via TGF-β signalling. Morphological analysis showed that gdf11 morphants and mutants displayed clear heart and liver laterality disorders in a Nodal signal-dependent manner. Additionally, we found that Kupffer's vesicle formation and ciliogenesis were impaired following gdf11 deletion. We also observed that Gdf11 may form a heterodimer with Spaw, which promotes Smad2/3 phosphorylation and activates TGF-β signalling. Subsequently, Gdf11 promotes left-right laterality by stimulating Foxj1a and its target gene expression. In summary, we reveal a critical role of Gdf11 in left-right patterning, providing fundamental insights into the developmental process of left-right asymmetry.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13765"},"PeriodicalIF":5.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459111","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}

引用次数: 0

Extraembryonic mesoderm cells derived from human embryonic stem cells rely on Wnt pathway activation. 人类胚胎干细胞衍生的胚外中胚层细胞依赖于 Wnt 途径的激活。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-09 DOI: 10.1111/cpr.13761

Si-Le Wang, Gao-Hui Shi, Kui Duan, Yu Yin, Tianqing Li

引用次数: 0

Modelling myocardial ischemia/reperfusion injury with inflammatory response in human ventricular cardiac organoids. 模拟心肌缺血/再灌注损伤与人心室心脏器官组织中的炎症反应

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-08 DOI: 10.1111/cpr.13762

Laihai Zhang, Yun Jiang, Wenwen Jia, Wenjun Le, Jie Liu, Peng Zhang, Huangtian Yang, Zhongmin Liu, Yang Liu

{"title":"Modelling myocardial ischemia/reperfusion injury with inflammatory response in human ventricular cardiac organoids.","authors":"Laihai Zhang, Yun Jiang, Wenwen Jia, Wenjun Le, Jie Liu, Peng Zhang, Huangtian Yang, Zhongmin Liu, Yang Liu","doi":"10.1111/cpr.13762","DOIUrl":"https://doi.org/10.1111/cpr.13762","url":null,"abstract":"Current therapeutic drug exploring targeting at myocardial ischemia/reperfusion (I/R) injury is limited due to the lack of humanized cardiac models that resemble myocardial damage and inflammatory response. Herein, we develop ventricular cardiac organoids from human induced pluripotent stem cells (hiPSCs) and simulate I/R injury by hypoxia/reoxygenation (H/R), which results in increased cardiomyocytes apoptosis, elevated oxidative stress, disrupted morphological structure and decreased beat amplitude. RNA-seq reveals a potential role of type I interferon (IFN-I) in this I/R injury model. We then introduce THP-1 cells and reveal inflammatory responses between monocytes/macrophages and H/R-induced ventricular cardiac organoids. Furthermore, we demonstrate Anifrolumab, an FDA approved antagonist of IFN-I receptor, effectively decreases IFN-I secretion and related gene expression, attenuates H/R-induced inflammation and oxidative stress in the co-culture system. This study advances the modelling of myocardial I/R injury with inflammatory response in human cardiac organoids, which provides a reliable platform for preclinical study and drug screening.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13762"},"PeriodicalIF":5.9,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388380","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}

引用次数: 0

Functional heterogeneity of meniscal fibrochondrocytes and microtissue models is dependent on modality of fibrochondrocyte isolation. 半月板纤维软骨细胞和微组织模型的功能异质性取决于纤维软骨细胞的分离方式。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-08 DOI: 10.1111/cpr.13735

Zhiyao Ma, Shikha Chawla, Xiaoyi Lan, Eva Zhou, Aillette Mulet-Sierra, Melanie Kunze, Mark Sommerfeldt, Adetola B Adesida

{"title":"Functional heterogeneity of meniscal fibrochondrocytes and microtissue models is dependent on modality of fibrochondrocyte isolation.","authors":"Zhiyao Ma, Shikha Chawla, Xiaoyi Lan, Eva Zhou, Aillette Mulet-Sierra, Melanie Kunze, Mark Sommerfeldt, Adetola B Adesida","doi":"10.1111/cpr.13735","DOIUrl":"https://doi.org/10.1111/cpr.13735","url":null,"abstract":"Collagenase digestion (d) and cellular outgrowth (og) are the current modalities of meniscus fibrochondrocytes (MFC) isolation for bioengineering and mechanobiology-related studies. However, the impact of these modalities on study outcomes is unknown. Here, we show that og- and d-isolated MFC have distinct proliferative capacities, transcriptomic profiles via RNA sequencing (RNAseq), extracellular matrix (ECM)-forming, and migratory capacities. Our data indicate that microtissue pellet models developed from og-isolated MFC display a contractile phenotype with higher expressions of alpha-smooth muscle actin (ACTA2) and transgelin (TAGLN) and are mechanically stiffer than their counterparts from d-MFC. Moreover, we introduce a novel method of MFC isolation designated digestion-after-outgrowth (dog). The transcriptomic profile of dog-MFC is distinct from d- and og-MFC, including a higher expression of mechanosensing caveolae-associated caveolin-1 (CAV1). Additionally, dog-MFC were superior chondrogenically and generated larger-size microtissue pellet models containing a higher frequency of smaller collagen fibre diameters. Thus, we demonstrate that the modalities of MFC isolation influence the downstream outcomes of bioengineering and mechanobiology-related studies.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13735"},"PeriodicalIF":5.9,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388378","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}

引用次数: 0

Deletion of Transmembrane protein 184b leads to retina degeneration in mice. 缺失跨膜蛋白 184b 会导致小鼠视网膜退化。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-07 DOI: 10.1111/cpr.13751

Guo Liu, Tiannan Liu, Junkai Tan, Xiaoyan Jiang, Yudi Fan, Kuanxiang Sun, Wenjing Liu, Xuyang Liu, Yeming Yang, Xianjun Zhu

{"title":"Deletion of Transmembrane protein 184b leads to retina degeneration in mice.","authors":"Guo Liu, Tiannan Liu, Junkai Tan, Xiaoyan Jiang, Yudi Fan, Kuanxiang Sun, Wenjing Liu, Xuyang Liu, Yeming Yang, Xianjun Zhu","doi":"10.1111/cpr.13751","DOIUrl":"https://doi.org/10.1111/cpr.13751","url":null,"abstract":"Transmembrane protein 184b (Tmem184b) has been implicated in axon degeneration and neuromuscular junction dysfunction. Notably, Tmem184b exhibits high expression levels in the retina; however, its specific function within this tissue remains poorly understood. To elucidate the role of Tmem184b in the mammalian visual system, we developed a Tmem184b knockout (KO) model for further investigation. Loss of Tmem184b led to significant decreases in both a and b wave amplitudes of scotopic electroretinogram (ERG) and reduced b wave amplitudes of photopic ERG, respectively, reflecting damage to both the photoreceptors and secondary neuronal cells of the retina. Histologic analyses showed a progressive retinal thinning accompanied by the significantly loss of retinal cells including cone, rod, bipolar, horizontal and retinal ganglion cells. The expression levels of photo-transduction-related proteins were down-regulated in KO retina. TUNEL (terminal deoxynucleotidyl transferase-mediated biotinylated Uridine-5'-triphosphate [UTP] nick end labelling) and glial fibrillary acidic protein (GFAP)-labelling results suggested the increased cell death and inflammation in the KO mice. RNA-sequencing analysis and GO enrichment analysis revealed that Tmem184b deletion resulted in down-regulated genes involved in various biological processes such as visual perception, response to hypoxia, regulation of transmembrane transporter activity. Taken together, our study revealed essential roles of Tmem184b in the mammalian retina and confirmed the underlying mechanisms including cell death, inflammation and hypoxia pathway in the absence of Tmem184b, providing a potential target for therapeutic and diagnostic development.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13751"},"PeriodicalIF":5.9,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388376","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}

引用次数: 0

Maternal infection with SARS-CoV-2 during early pregnancy induces hypoxia at the maternal-fetal interface. 孕早期母体感染 SARS-CoV-2 会导致母胎界面缺氧。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-07 DOI: 10.1111/cpr.13749

Xiaohui Shi, Chenxiang Xi, Baoxing Dong, Zihui Yan, Wenqiang Liu, Shaorong Gao, Di Chen

{"title":"Maternal infection with SARS-CoV-2 during early pregnancy induces hypoxia at the maternal-fetal interface.","authors":"Xiaohui Shi, Chenxiang Xi, Baoxing Dong, Zihui Yan, Wenqiang Liu, Shaorong Gao, Di Chen","doi":"10.1111/cpr.13749","DOIUrl":"https://doi.org/10.1111/cpr.13749","url":null,"abstract":"The coronavirus disease 2019 (COVID-19) pandemic increases the risk of adverse fetal outcomes during pregnancy. Maternal infection during pregnancy, particularly with cytomegalovirus (CMV), hepatitis B and C virus, and human immunodeficiency virus can have detrimental effects on both mother and fetus, potentially leading to adverse outcomes such as spontaneous abortion or neonatal infection. However, the impact of severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection on the maternal-fetal interface remains poorly understood. In this study, we initially utilised immunofluorescence and immunohistochemical to investigate placental samples from pregnant women who were infected with SARS-CoV-2 during the first trimester. Our data indicate that infection in the first trimester induces an upregulation of hypoxia inducible factor (HIF) levels at the maternal-fetal interface. Subsequently, single-cell RNA sequencing and metabolomics sequencing analyses reveal alterations in maternal-fetal interface. Remarkably, immune cells exhibited low expression levels of HIF possibly associated with immune activation. Furthermore, our findings demonstrate a gradual reduction in transcriptome and metabolic changes as gestation progressed beyond 12-16 weeks compared to samples obtained at 6-8 weeks gestation. Overall, our study suggests that early-stage SARS-CoV-2 infection during the first trimester leads to severe hypoxia and aberrant cell metabolism at the maternal-fetal interface which gradually resolves as pregnancy progresses. Nevertheless, these abnormal changes may have long-term implications for maternal-fetal interface development.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13749"},"PeriodicalIF":5.9,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388379","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}

引用次数: 0

KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function. KDM2B 及其多肽通过干预 EZH2 的功能促进大鼠顶端乳头介导的神经损伤修复干细胞。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-02 DOI: 10.1111/cpr.13756

Yangyang Cao, Yantong Wang, Dengsheng Xia, Zhipeng Fan

{"title":"KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function.","authors":"Yangyang Cao, Yantong Wang, Dengsheng Xia, Zhipeng Fan","doi":"10.1111/cpr.13756","DOIUrl":"https://doi.org/10.1111/cpr.13756","url":null,"abstract":"How to improve the neurogenic potential of mesenchymal stem cells (MSCs) and develop biological agent based on the underlying epigenetic mechanism remains a challenge. Here, we investigated the effect of histone demethylase Lysine (K)-specific demethylase 2B (KDM2B) on neurogenic differentiation and nerve injury repair by using MSCs from dental apical papilla (SCAP). We found that KDM2B promoted the neurogenic indicators expression and neural spheres formation in SCAP, and modified the Histone H3K4 trimethylation (H3K4me3) methylation on neurogenesis-related genes. KDM2B improved the SCAP mediated recovery of motor ability at the early healing stage of spinal cord injury rats. Meanwhile, KDM2B acted as a negative regulator to its partner EZH2 during neurogenic differentiation, enhancer of zeste homologue 2 (EZH2) suppressed the neurogenic ability of SCAP. Further, the protein interaction between KDM2B and EZH2 was identified which decreased during neurogenic differentiation. On this basis, we revealed seven key protein binding sequences of KDM2B to EZH2, and synthesized KDM2B-peptides based on these sequences. By the usage of KDM2B-peptides, EZH2 function was effectively intervened and the neurogenic ability of SCAP was promoted. More, KDM2B-peptides significantly improved the SCAP mediated functional recovery at SCI early phase. Our study revealed that KDM2B acted as a promotor to neurogenic differentiation ability of dental MSCs through binding and negatively regulating EZH2, and provided the KDM2B-peptides as candidate agents for improving the neurogenic ability of MSCs and nerve injury repair.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13756"},"PeriodicalIF":5.9,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364564","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}

引用次数: 0

Mechanisms and therapeutic potential of disulphidptosis in cancer. 癌症中的二硫化钼机制和治疗潜力。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-01 DOI: 10.1111/cpr.13752

Yanhu Li, Haijun Zhang, Fengguang Yang, Daxue Zhu, Shijie Chen, Zhaoheng Wang, Ziyan Wei, Zhili Yang, Jingwen Jia, Yizhi Zhang, Dongxin Wang, Mingdong Ma, Xuewen Kang

{"title":"Mechanisms and therapeutic potential of disulphidptosis in cancer.","authors":"Yanhu Li, Haijun Zhang, Fengguang Yang, Daxue Zhu, Shijie Chen, Zhaoheng Wang, Ziyan Wei, Zhili Yang, Jingwen Jia, Yizhi Zhang, Dongxin Wang, Mingdong Ma, Xuewen Kang","doi":"10.1111/cpr.13752","DOIUrl":"https://doi.org/10.1111/cpr.13752","url":null,"abstract":"SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction-oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F-actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis-based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13752"},"PeriodicalIF":5.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364566","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}

引用次数: 0