Cell Proliferation最新文献_第3页

Matrix stiffness regulates mitochondria-lysosome contacts to modulate the mitochondrial network, alleviate the senescence of MSCs. 基质硬度调节线粒体-溶酶体接触，从而调节线粒体网络，缓解间充质干细胞的衰老。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-10-01 DOI: 10.1111/cpr.13746

Kang Wang, Chingchun Ho, Xiangyu Li, Jianfeng Hou, Qipei Luo, Jiahong Wu, Yuxin Yang, Xinchun Zhang

{"title":"Matrix stiffness regulates mitochondria-lysosome contacts to modulate the mitochondrial network, alleviate the senescence of MSCs.","authors":"Kang Wang, Chingchun Ho, Xiangyu Li, Jianfeng Hou, Qipei Luo, Jiahong Wu, Yuxin Yang, Xinchun Zhang","doi":"10.1111/cpr.13746","DOIUrl":"https://doi.org/10.1111/cpr.13746","url":null,"abstract":"The extracellular microenvironment encompasses the extracellular matrix, neighbouring cells, cytokines, and fluid components. Anomalies in the microenvironment can trigger aging and a decreased differentiation capacity in mesenchymal stem cells (MSCs). MSCs can perceive variations in the firmness of the extracellular matrix and respond by regulating mitochondrial function. Diminished mitochondrial function is intricately linked to cellular aging, and studies have shown that mitochondria-lysosome contacts (M-L contacts) can regulate mitochondrial function to sustain cellular equilibrium. Nonetheless, the influence of M-L contacts on MSC aging under varying matrix stiffness remains unclear. In this study, utilizing single-cell RNA sequencing and atomic force microscopy, we further demonstrate that reduced matrix stiffness in older individuals leads to MSC aging and subsequent decline in osteogenic ability. Mechanistically, augmented M-L contacts under low matrix stiffness exacerbate MSC aging by escalating mitochondrial oxidative stress and peripheral division. Moreover, under soft matrix stiffness, cytoskeleton reorganization facilitates rapid movement of lysosomes. The M-L contacts inhibitor ML282 ameliorates MSC aging by reinstating mitochondrial network and function. Overall, our findings confirm that MSC aging is instigated by disruption of the mitochondrial network and function induced by matrix stiffness, while also elucidating the potential mechanism by which M-L Contact regulates mitochondrial homeostasis. Crucially, this presents promise for cellular anti-aging strategies centred on mitochondria, particularly in the realm of stem cell therapy.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13746"},"PeriodicalIF":5.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364565","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

Notch-1 regulates collective breast cancer cell migration by controlling intercellular junction and cytoskeletal organization. Notch-1通过控制细胞间连接和细胞骨架组织来调节乳腺癌细胞的集体迁移。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-29 DOI: 10.1111/cpr.13754

Yixi Zhang, Xiang Qin, Ronghua Guo, Xiyue Sun, Zihan Zhao, Hanyu Guo, Meng Wang, Shun Li, Tingting Li, Dong Lv, Yiyao Liu

{"title":"Notch-1 regulates collective breast cancer cell migration by controlling intercellular junction and cytoskeletal organization.","authors":"Yixi Zhang, Xiang Qin, Ronghua Guo, Xiyue Sun, Zihan Zhao, Hanyu Guo, Meng Wang, Shun Li, Tingting Li, Dong Lv, Yiyao Liu","doi":"10.1111/cpr.13754","DOIUrl":"https://doi.org/10.1111/cpr.13754","url":null,"abstract":"Pathological observations show that cancer cells frequently invade the surrounding normal tissue in collective rather than individual cell migration. However, general principles governing collective cell migration remain to be discovered. Different from individual cell migration, we demonstrated that the Notch-1-activation reduced collective cells speed and distances. In particular, Notch-1-activation induced cellular cytoskeletal remodelling, strengthened the intercellular junctions and cell-matrix adhesions. Mechanistically, Notch-1 activation prevented the phosphorylation of GSK-3β and the translocation of cytoplasmic free β-catenin to the nucleus, which increased E-cadherin expression and tight intercellular junctions. Moreover, Notch-1 signalling also activated the RhoA/ROCK pathway, promoting reorganization of F-actin and contractile forces produced by myosin. Further, Notch-1 activation increased cell adhesion to the extracellular substrate, which inhibited collective cell migration. These findings highlight that cell adhesions and cell-cell junctions contribute to collective cell migration and provide new insights into mechanisms of the modulation of Notch-1 signalling pathway on cancer cell malignancy.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13754"},"PeriodicalIF":5.9,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342557","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

Nanoemulsion-based transdermal delivery of third-generation steroidal and non-steroidal aromatase inhibitors in preclinical models. 基于纳米乳液的第三代类固醇和非类固醇芳香化酶抑制剂在临床前模型中的透皮给药。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-29 DOI: 10.1111/cpr.13753

Lanyang Gao, Lin Gao, Shiyao Huang, Lei Sun, Mei Li, Chen Shen, Youyou Chen, Ruihao Tan, Yuji Chen, Chengguo Zhan, Frank Heinrich Wieland, Yingying Liu, Yinan Zhang, Yao Luo

{"title":"Nanoemulsion-based transdermal delivery of third-generation steroidal and non-steroidal aromatase inhibitors in preclinical models.","authors":"Lanyang Gao, Lin Gao, Shiyao Huang, Lei Sun, Mei Li, Chen Shen, Youyou Chen, Ruihao Tan, Yuji Chen, Chengguo Zhan, Frank Heinrich Wieland, Yingying Liu, Yinan Zhang, Yao Luo","doi":"10.1111/cpr.13753","DOIUrl":"https://doi.org/10.1111/cpr.13753","url":null,"abstract":"Aromatase inhibitors are effective in treating hormone receptor-positive breast cancer, particularly in postmenopausal women. However, the challenges of inconsistent dissolution, variable absorption and side effects with oral administration persist. To address these issues, transdermal delivery has emerged as a viable alternative. In our study, we have developed nanoemulsion-based transdermal creams containing third-generation aromatase inhibitors Exemestane (EXE) or Letrozole (LE) and evaluated their toxicity, anti-tumour effects and androgenic potency using preclinical models including Bama minipigs, DMBA-induced breast cancer rats and orchidectomized male rats. The results of our study are significant, suggesting that both creams effectively penetrated the skin, demonstrating an impressive anti-breast cancer effect. Importantly, EXE cream had no organ toxicity at the tested dose, providing a reassuring safety profile for its use. In contrast, LE cream displayed reversible toxicity from drug molecule itself in animals at the given dose, dissipating after 3 weeks of withdrawal and recovery. This study establishes a solid foundation for the safe clinical use of third-generation aromatase inhibitors. It highlights transdermal creams as a promising drug delivery carrier for administering them.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13753"},"PeriodicalIF":5.9,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342556","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

Dynamic transcriptomic and regulatory networks underpinning the transition from fetal primordial germ cells to spermatogonia in mice. 支撑小鼠从胎儿原始生殖细胞向精原细胞过渡的动态转录组和调控网络。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-27 DOI: 10.1111/cpr.13755

Jiexiang Zhao, Kang Tang, Gurong Jiang, Xinyan Yang, Manman Cui, Cong Wan, Zhaoxiang Ouyang, Yi Zheng, Zhaoting Liu, Mei Wang, Xiao-Yang Zhao, Gang Chang

{"title":"Dynamic transcriptomic and regulatory networks underpinning the transition from fetal primordial germ cells to spermatogonia in mice.","authors":"Jiexiang Zhao, Kang Tang, Gurong Jiang, Xinyan Yang, Manman Cui, Cong Wan, Zhaoxiang Ouyang, Yi Zheng, Zhaoting Liu, Mei Wang, Xiao-Yang Zhao, Gang Chang","doi":"10.1111/cpr.13755","DOIUrl":"https://doi.org/10.1111/cpr.13755","url":null,"abstract":"The transition from fetal primordial germ cells (PGCs) to spermatogonia (SPG) is critical for male germ cell development; however, the detailed transcriptomic dynamics and regulation underlying this transition remain poorly understood. Here by interrogating the comprehensive transcriptome atlas dataset of mouse male germ cells and gonadal cells development, we elucidated the regulatory networks underlying this transition. Our single-cell transcriptome analysis revealed that the transition from PGCs to SPG was characterized by global hypertranscription. A total of 315 highly active regulators were identified to be potentially involved in this transition, among which a non-transcription factor (TF) regulator TAGLN2 was validated to be essential for spermatogonial stem cells (SSCs) maintenance and differentiation. Metabolism profiling analysis also revealed dynamic changes in metabolism-related gene expression during PGC to SPG transition. Furthermore, we uncovered that intricate cell-cell communication exerted potential functions in the regulation of hypertranscription in germ cells by collaborating with stage-specific active regulators. Collectively, our work extends the understanding of molecular mechanisms underlying male germ cell development, offering insights into the recapitulation of germ cell generation in vitro.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13755"},"PeriodicalIF":5.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342552","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

Flavonoid chrysin activates both TrkB and FGFR1 receptors while upregulates their endogenous ligands such as brain derived neurotrophic factor to promote human neurogenesis. 黄酮类化合物菊黄素可激活 TrkB 和 FGFR1 受体，同时上调它们的内源性配体，如脑源性神经营养因子，从而促进人类神经发生。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-27 DOI: 10.1111/cpr.13732

Xiaoxu Dong, Gang Pei, Zhuo Yang, Shichao Huang

{"title":"Flavonoid chrysin activates both TrkB and FGFR1 receptors while upregulates their endogenous ligands such as brain derived neurotrophic factor to promote human neurogenesis.","authors":"Xiaoxu Dong, Gang Pei, Zhuo Yang, Shichao Huang","doi":"10.1111/cpr.13732","DOIUrl":"https://doi.org/10.1111/cpr.13732","url":null,"abstract":"Neurogenesis is the process of generating new neurons from neural stem cells (NSCs) and plays a crucial role in neurological diseases. The process involves a series of steps, including NSC proliferation, migration and differentiation, which are regulated by multiple pathways such as neurotrophic Trk and fibroblast growth factor receptors (FGFR) signalling. Despite the discovery of numerous compounds capable of modulating individual stages of neurogenesis, it remains challenging to identify an agent that can regulate multiple cellular processes of neurogenesis. Here, through screening of bioactive compounds in dietary functional foods, we identified a flavonoid chrysin that not only enhanced the human NSCs proliferation but also facilitated neuronal differentiation and neurite outgrowth. Further mechanistic study revealed the effect of chrysin was attenuated by inhibition of neurotrophic tropomyosin receptor kinase-B (TrkB) receptor. Consistently, chrysin activated TrkB and downstream ERK1/2 and AKT. Intriguingly, we found that the effect of chrysin was also reduced by FGFR1 blockade. Moreover, extended treatment of chrysin enhanced levels of brain-derived neurotrophic factor, as well as FGF1 and FGF8. Finally, chrysin was found to promote neurogenesis in human cerebral organoids by increasing the organoid expansion and folding, which was also mediated by TrkB and FGFR1 signalling. To conclude, our study indicates that activating both TrkB and FGFR1 signalling could be a promising avenue for therapeutic interventions in neurological diseases, and chrysin appears to be a potential candidate for the development of such treatments.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13732"},"PeriodicalIF":5.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342553","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

miR-27a-3p regulates intestinal cell proliferation and differentiation through Wnt/β-catenin signalling. miR-27a-3p 通过 Wnt/β-catenin 信号调节肠细胞的增殖和分化。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-27 DOI: 10.1111/cpr.13757

Chang Li, Yuning Zhou, Yinping Jiang, Zhijie Yin, Heidi L Weiss, Qingding Wang, B Mark Evers

{"title":"miR-27a-3p regulates intestinal cell proliferation and differentiation through Wnt/β-catenin signalling.","authors":"Chang Li, Yuning Zhou, Yinping Jiang, Zhijie Yin, Heidi L Weiss, Qingding Wang, B Mark Evers","doi":"10.1111/cpr.13757","DOIUrl":"https://doi.org/10.1111/cpr.13757","url":null,"abstract":"Intestinal stem cells differentiate into absorptive enterocytes, characterised by increased brush border enzymes such as intestinal alkaline phosphatase (IAP), making up the majority (95%) of the terminally differentiated cells in the villus. Loss of integrity of the intestinal epithelium plays a key role in inflammatory diseases and gastrointestinal infection. Here, we show that the intestinal microRNA (miR)-27a-3p is an important regulator of intestinal epithelial cell proliferation and enterocyte differentiation. Repression of endogenous miR-27a-3p leads to increased enterocyte differentiation and decreased intestinal epithelial cell proliferation in mouse and human small intestinal organoids. Mechanistically, miR-27a-3p regulates intestinal cell differentiation and proliferation at least in part through the regulation of retinoic acid receptor α (RXRα), a modulator of Wnt/β-catenin signalling. Repression of miR-27a-3p increases the expression of RXRα and concomitantly, decreases the expression of active β-catenin and cyclin D1. In contrast, overexpression of miR-27a-3p mimic decreases the expression of RXRα and increases the expression of active β-catenin and cyclin D1. Moreover, overexpression of the miR-27a-3p mimic results in impaired enterocyte differentiation and increases intestinal epithelial cell proliferation. These alterations were attenuated or blocked by Wnt inhibition. Our study demonstrates an miR-27a-3p/RXRα/Wnt/β-catenin pathway that is important for the maintenance of enterocyte homeostasis in the small intestine.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13757"},"PeriodicalIF":5.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342555","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

Inactivation of JNK signalling results in polarity loss and cell senescence of Sertoli cell. JNK 信号失活会导致 Sertoli 细胞极性丧失和细胞衰老。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-27 DOI: 10.1111/cpr.13760

Zhiming Shen, Yang Gao, Xuedong Sun, Min Chen, Changhuo Cen, Mengyue Wang, Nan Wang, Bowen Liu, Jiayi Li, Xiuhong Cui, Jian Hou, Yuhua Shi, Fei Gao

{"title":"Inactivation of JNK signalling results in polarity loss and cell senescence of Sertoli cell.","authors":"Zhiming Shen, Yang Gao, Xuedong Sun, Min Chen, Changhuo Cen, Mengyue Wang, Nan Wang, Bowen Liu, Jiayi Li, Xiuhong Cui, Jian Hou, Yuhua Shi, Fei Gao","doi":"10.1111/cpr.13760","DOIUrl":"https://doi.org/10.1111/cpr.13760","url":null,"abstract":"As major somatic cells in the testis, Sertoli cell development is precisely regulated by numerous factors, and aberrant development of these cells is associated with male reproductive diseases. JNK signalling is evolutionarily conserved and involved in multiple critical biological processes. Here, we found that the double knockout of Jnk1 and Jnk2 resulted in aberrant localisation of Sertoli cells at early developmental stages, with most Sertoli cells being lost at later stages. Further studies revealed that the inactivation of JNK signalling caused polarity loss in Sertoli cells. In vitro-cultured Jnk1/2-DKO Sertoli cells exhibited a senescence-associated phenotype. Mechanistic studies demonstrate that JNK signalling is likely involved in establishing Sertoli cell polarity by regulating the expression of TGF-β2, mediated by c-Jun. The senescence of Sertoli cells in JNKs-deficient mice is caused by aberrant proteolysis of P27KIP1, mediated by c-Myc. This study demonstrates the role of JNK signalling in Sertoli cell development and functional maintenance, which may also represent an aetiology of male infertility in humans.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13760"},"PeriodicalIF":5.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342554","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

Correction to ‘BMAL1 deficiency promotes skeletal mandibular hypoplasia via OPG downregulation’ 对 "BMAL1缺乏症通过OPG下调促进骨骼下颌骨发育不良 "的更正

IF 8.5 1区生物学

Cell Proliferation Pub Date : 2024-09-20 DOI: 10.1111/cpr.13750

引用次数: 0

Role of Wnt5a in modulation of osteoporotic adipose-derived stem cells and osteogenesis Wnt5a 在调节骨质疏松性脂肪来源干细胞和成骨过程中的作用

IF 8.5 1区生物学

Cell Proliferation Pub Date : 2024-09-17 DOI: 10.1111/cpr.13747

Lin Liu, Shihong Luo, Qiumei Li, Kui Huang, Yuan Jiang, Lu Zeng, Xiaorong Lan, Qing Li, Jingang Xiao

{"title":"Role of Wnt5a in modulation of osteoporotic adipose-derived stem cells and osteogenesis","authors":"Lin Liu, Shihong Luo, Qiumei Li, Kui Huang, Yuan Jiang, Lu Zeng, Xiaorong Lan, Qing Li, Jingang Xiao","doi":"10.1111/cpr.13747","DOIUrl":"https://doi.org/10.1111/cpr.13747","url":null,"abstract":"Osteoporosis, a condition marked by the deterioration of bone microarchitecture and increased facture risk, arises from a disruption in bone metabolism, with osteoclasts surpassing osteoblasts in bone resorption versus formation. The Wnt signalling pathway, a key regulator of bone maintenance, remains partially understood in osteoporosis. Our research delves into the role of Wnt-related molecules in this disease. In osteoporotic adipose-derived stem cells (OP-ASCs), we detected a significant decrease in Ctnnb1 and Frizzled-6 (Fzd6), contrasted by an increase in Gsk-3β and Wnt5a. Activation of the Wnt pathway by LiCl resulted in elevated Ctnnb1 and Fzd6, but decreased Gsk-3β and Wnt5a levels, promoting OP-ASCs' bone-formation capacity. In contrast, inhibition of this pathway by DKK-1 led to diminished Ctnnb1 and Fzd6, and increased Gsk-3β and Wnt5a, adversely affecting osteogenesis. Furthermore, our findings show that overexpressing Wnt5a impedes, while silencing it enhances the bone-forming capability of OP-ASCs. In a cranial bone defect model, the implantation of Wnt5a-silenced OP-ASCs with biphasic calcium phosphate scaffolds significantly promoted new bone formation. These observations indicated a repression of the canonical Wnt pathway and a stimulation of the non-canonical pathway in OP-ASCs. Silencing Wnt5a increased the osteogenic and regenerative abilities of OP-ASCs. Our study suggests targeting Wnt5a could be a promising strategy for enhancing bone regeneration in post-menopausal osteoporosis.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"64 1","pages":""},"PeriodicalIF":8.5,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142268006","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

RETRACTION: Legionella Pneumophila Infection Reduces the Mitochondrial Membrane Potential Through Lpg2444-Inhibited Mitocytosis 返回：嗜肺军团菌感染通过 Lpg2444 抑制的有丝分裂降低线粒体膜电位

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2024-09-15 DOI: 10.1111/cpr.13748

引用次数: 0