Journal of Cell Communication and Signaling最新文献_第4页

Role of the calcium-sensing receptor in regulating vascular function 钙敏感受体在调节血管功能中的作用

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-02-05 DOI: 10.1002/ccs3.70004

Anthony P. Albert, Harry Z.E. Greenberg

{"title":"Role of the calcium-sensing receptor in regulating vascular function","authors":"Anthony P. Albert, Harry Z.E. Greenberg","doi":"10.1002/ccs3.70004","DOIUrl":"https://doi.org/10.1002/ccs3.70004","url":null,"abstract":"Functional expression of the calcium-sensing receptor (CaSR) in calcitropic tissues, for example, parathyroid glands and kidneys, is important for maintaining Ca2+ homeostasis. It is also established that the CaSR is present in tissues previously thought to be noncalcitropic and this review discusses the role of the CaSR in vascular function, focusing mainly on contractility but also outlining its role in cell proliferation and calcification. Stimulation of the CaSR by extracellular Ca2+ concentration ([Ca2+]o) on perivascular sensory nerves and vascular endothelial cells is associated with vasodilatation through the release of vasoactive substances and stimulation of IKCa channels and nitric oxide synthesis, respectively, which mediate endothelium-derived hyperpolarizations and activation of BKCa channels and KATP channels in vascular smooth muscle cells (VSMCs). CaSR-induced vasoconstrictions are mediated by the CaSR expressed in VSMCs, which are coupled to the Gq/11 protein-coupled pathway. In addition, the CaSR expressed on VSMCs also regulates proliferation and calcification. Consequently, the CaSR has been implicated in regulating systemic and pulmonary blood pressure and calcimimetics and calcilytics are potential therapeutic targets for cardiovascular diseases, such as hypertension, pulmonary artery hypertension, and atherosclerosis.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143248753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CCN2 functions as a modulator of cell cycle regulation in human dermal fibroblasts CCN2在人真皮成纤维细胞中发挥细胞周期调节的作用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-02-01 DOI: 10.1002/ccs3.70003

Taihao Quan, Yuan Shao, Trupta Purohit, Yiou Jiang, Zhaoping Qin, Gary J. Fisher, Nathan H. Lents, Joseph J. Baldassare

{"title":"CCN2 functions as a modulator of cell cycle regulation in human dermal fibroblasts","authors":"Taihao Quan, Yuan Shao, Trupta Purohit, Yiou Jiang, Zhaoping Qin, Gary J. Fisher, Nathan H. Lents, Joseph J. Baldassare","doi":"10.1002/ccs3.70003","DOIUrl":"10.1002/ccs3.70003","url":null,"abstract":"CCN2 is widely regarded as a profibrotic factor involved in fibrotic disorders by regulating extracellular matrix (ECM). We report here that CCN2 functions as a critical cell cycle regulator in primary human dermal fibroblasts (HDFs). siRNA-mediated knockdown of CCN2 halted proliferation of primary HDFs, which was rescued by a siRNA-resistant CCN2 expression vector. Furthermore, CCN2 knockdown caused a significant accumulation of cells in G1/G0 phase and blocked entry into S-phase. Mechanistically, CCN2 knockdown blocked cyclin E and CDK4/cyclin D nuclear translocation, and abrogated CDK2 activity. Markedly, CCN2 translocated to the nucleus and co-localized with cyclin D1 upon cell cycle stimulation. Finally, we show that CCN2, a bona fide YAP/TAZ target gene, partially mediates YAP/TAZ-dependent proliferation of primary HDFs. These data provide evidence of a novel CCN2 function as a cell cycle regulator in primary HDFs proliferation, in addition to its known role in ECM regulation.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The opposite effect of ELP4 and ZEB2 on TCF7L2-mediated microglia polarization in ischemic stroke ELP4和ZEB2对缺血性脑卒中tcf7l2介导的小胶质细胞极化的相反作用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-01-16 DOI: 10.1002/ccs3.12061

Xiao-li Min, Sixian Lin, Jia-yi Hu, Rui Jing, Qing Zhao, Fei-fei Shang, Yong Zeng

{"title":"The opposite effect of ELP4 and ZEB2 on TCF7L2-mediated microglia polarization in ischemic stroke","authors":"Xiao-li Min, Sixian Lin, Jia-yi Hu, Rui Jing, Qing Zhao, Fei-fei Shang, Yong Zeng","doi":"10.1002/ccs3.12061","DOIUrl":"10.1002/ccs3.12061","url":null,"abstract":"Microglia M1 polarization plays important role in the development of ischemic stroke (IS). This study explored the role of transcription factor 7 like 2 (TCF7L2) in regulating microglia M1 polarization during IS. TTC staining was used to determine the cerebral infarction, and Nissl staining was applied to examine neuronal injury. The secretion levels of cytokines were measured using ELISA. The interaction between Zinc finger E-Box binding homeobox 2 (ZEB2) and TCF7L2 was analyzed by Co-IP, and H3K27ac enrichment in the TCF7L2 promoter was detected by ChIP assay. TCF7L2 knockdown reduced MCAO/R-induced mice cerebral injury. TCF7L2 silencing or TAK-242 (TLR4 antagonist) injection inhibited OGD/R-induced microglia M1 polarization by repressing the TLR4/NF-κB signal, and TCF7L2 knockdown combined with TAK-242 treatment further inhibited microglia M1 polarization. TCF7L2 promoted transcriptional activation of TLR4. ELP4 enhanced H3K27ac-mediated transcriptional activation of TCF7L2, and ZEB2 promoted the K48-linked ubiquitination of TCF7L2. TCF7L2 overexpression abolished the inhibitory effect of ELP4 knockdown or ZEB2 overexpression on OGD/R-induced microglia M1 polarization. TCF7L2 exacerbated cerebral injury by promoting microglia M1 polarization during IS progression. Mechanistically, ELP4 promoted TCF7L2 expression by promoting H3K27ac enrichment in the TCF7L2 promoter, while ZEB2 promoted TCF7L2 ubiquitination degradation.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

I had a dream 我做了一个梦。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-01-13 DOI: 10.1002/ccs3.12064

Bernard Perbal

引用次数: 0

M2-polarized tumor-associated macrophage-secreted exosomal lncRNA NEAT1 upregulates galectin-3 by recruiting KLF5 and promotes HCC immune escape m2极化肿瘤相关巨噬细胞分泌外泌体lncRNA NEAT1通过募集KLF5上调半凝集素-3，促进HCC免疫逃逸。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-12-23 DOI: 10.1002/ccs3.12060

Wei Yuan, Qigang Sun, Xiaodan Zhu, Bo Li, Yongping Zou, Zhehao Liu

{"title":"M2-polarized tumor-associated macrophage-secreted exosomal lncRNA NEAT1 upregulates galectin-3 by recruiting KLF5 and promotes HCC immune escape","authors":"Wei Yuan, Qigang Sun, Xiaodan Zhu, Bo Li, Yongping Zou, Zhehao Liu","doi":"10.1002/ccs3.12060","DOIUrl":"10.1002/ccs3.12060","url":null,"abstract":"HCC cell immune escape is a critical element in the evolution of HCC malignancy. Herein, the regulatory mechanism of lncRNA NEAT1 in regulating HCC immune escape was investigated. Exosomes were isolated from M2 TAMs using ExoQuick-TC. Then, HCC cells were incubated with M2 TAMs-derived exosomes (M2-exos). The activation of perforin+CD8+ T cells was measured using flow cytometry. The secretion of IFN-γ was assessed using ELISA. Cell viability and migration were detected using CCK8 and Transwell assays, respectively. RIP and RNA pull-down assays were used to investigate the link between NEAT1 and KLF5. ChIP and dual-luciferase reporter assays were used to investigate the interaction between KLF5 and the LGALS3 promoter. Our results showed that NEAT1, KLF5 and galectin-3 were overexpressed in HCC tissues. M2-exos treatment promoted HCC proliferation, migration, and immune escape. It was found that NEAT1 was enriched in M2-TAMs and M2-exos. M2-exos facilitated HCC immune escape, whereas NEAT1 silencing reversed this effect. NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5. Mechanically, M2-TAM-derived exosomal NEAT1 induced HCC immune escape by upregulating KLF5/galectin-3 axis. M2-TAM-derived exosomal NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5 to promote perforin+CD8+ T cell depletion and further accelerate HCC immune escape.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11666343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Characterization of microRNA-223-3p as a novel promoter of cell proliferation and invasion in papillary thyroid carcinoma microRNA-223-3p作为甲状腺乳头状癌细胞增殖和侵袭的新型启动子的特征描述

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-12-19 DOI: 10.1002/ccs3.12057

Xinghe Pan, Junliang Liu, Yitong Zhang, Chenglin Sun, You Li, Hongpeng Guo

引用次数: 0

The small molecule peptide ANXA114-26 inhibits ovarian cancer cell proliferation and reverses cisplatin resistance by binding to the formyl peptide receptors receptor 小分子肽ANXA114-26通过与甲酰基肽受体结合抑制卵巢癌细胞增殖并逆转顺铂耐药性

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-12-19 DOI: 10.1002/ccs3.12058

Nana Li, Peihua Yan, Ling Guo, Huiyan Wang, Baohong Cui, Lichen Teng, Yajuan Su

{"title":"The small molecule peptide ANXA114-26 inhibits ovarian cancer cell proliferation and reverses cisplatin resistance by binding to the formyl peptide receptors receptor","authors":"Nana Li, Peihua Yan, Ling Guo, Huiyan Wang, Baohong Cui, Lichen Teng, Yajuan Su","doi":"10.1002/ccs3.12058","DOIUrl":"https://doi.org/10.1002/ccs3.12058","url":null,"abstract":"Chemo-resistance in ovarian cancer is currently a major obstacle to the treatment and recovery of ovarian cancer. Therefore, identifying factors associated with chemo-resistance in ovarian cancer may reverse chemo-sensitization. Using isobaric tags for relative and absolute quantitation (ITRAQ) technology, we found a small molecule peptide with annexin 1 (ANXA1) as a precursor protein. Then, we explored the effects and mechanisms of this small molecule peptide on the proliferation, apoptosis, and drug resistance of ovarian cancer resistant cells through CCK-8, EdU cell proliferation assay, Annexin V-FITC/PI assay, Western blot,qRT-PCR. ANXA114-26 was highly expressed in the serums of sensitive patients. ANXA114-26 promoted apoptosis of ovarian cancer cells and increased the sensitization of ovarian cancer cells to cisplatin. The ANXA114-26 and ANXA1 competitively bind formyl peptide receptors (FPR). ANXA114-26 decreased multidrug resistance-associated protein 1 (MRP1) expression in ovarian cancer cells through the FPR/Cyclin D1/NF-ĸBp65 pathway. We found a peptide derived named ANXA114-26 in the serum of ovarian cancer patients. It can reduce ovarian cancer cell proliferation and reduce MRP1 expression through the FPR/Cyclin D1/NF-ĸBp65 pathway.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142868711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The case of Connective Tissue Growth Factor and the pit of misleading and improper nomenclatures 结缔组织生长因子的案例和误导性不当命名的隐患

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-12-19 DOI: 10.1002/ccs3.12062

Bernard Perbal

引用次数: 0

Cytokine expression and cytokine-mediated cell–cell communication during skeletal muscle regeneration revealed by integrative analysis of single-cell RNA sequencing data 单细胞RNA测序数据的综合分析揭示了骨骼肌再生过程中细胞因子表达和细胞因子介导的细胞间通讯。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-12-04 DOI: 10.1002/ccs3.12055

Pallob Barai, Jie Chen

{"title":"Cytokine expression and cytokine-mediated cell–cell communication during skeletal muscle regeneration revealed by integrative analysis of single-cell RNA sequencing data","authors":"Pallob Barai, Jie Chen","doi":"10.1002/ccs3.12055","DOIUrl":"10.1002/ccs3.12055","url":null,"abstract":"Skeletal muscles undergo self-repair upon injury, owing to the resident muscle stem cells and their extensive communication with the microenvironment of injured muscles. Cytokines play a critical role in orchestrating intercell communication to ensure successful regeneration. Immune cells as well as other types of cells in the injury site, including muscle stem cells, are known to secret cytokines. However, the extent to which various cell types express distinct cytokines and how the secreted cytokines are involved in intercell communication during regeneration are largely unknown. Here we integrated 15 publicly available single-cell RNA-sequencing (scRNA-seq) datasets of mouse skeletal muscles at early regeneration timepoints (0, 2, 5, and 7 days after injury). The resulting dataset was analyzed for the expression of 393 annotated mouse cytokines. We found widespread and dynamic cytokine expression by all cell types in the regenerating muscle. Interrogating the integrated dataset using CellChat revealed extensive, bidirectional cell–cell communications during regeneration. Our findings provide a comprehensive view of cytokine signaling in the regenerating muscle, which can guide future studies of ligand-receptor signaling and cell–cell interaction to achieve new mechanistic insights into the regulation of muscle regeneration.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prognosis and diagnosis prediction of lung adenocarcinoma outcome based on a novel model anchored in circadian clock-related genes 基于生物钟相关基因新模型的肺腺癌预后和诊断预测。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-11-13 DOI: 10.1002/ccs3.12053

Bernard Perbal

引用次数: 0