ArticleCell proliferation2008
Silence of ClC-3 chloride channel inhibits cell proliferation and the cell cycle via G/S phase arrest in rat basilar arterial smooth muscle cells.
Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 66 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- LRRC8A is essential for volume-regulated anion channel in smooth muscle cells contributing to cerebrovascular remodeling during hypertension.Cell proliferation · 2021Article
- SGK1 mediates the hypotonic protective effect against HActa pharmacologica Sinica · 2020Article
- NPPB prevents postoperative peritoneal adhesion formation by blocking volume-activated ClNaunyn-Schmiedeberg's archives of pharmacology · 2020Article
- The chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) controls cellular quiescence by hyperpolarizing the cell membrane during diapause in the crustaceanThe Journal of biological chemistry · 2019Article
- Article
- Knockdown of Chloride Channel-3 Inhibits Breast Cancer GrowthJournal of breast cancer · 2018Article
- WNK1 is required for proliferation induced by hypotonic challenge in rat vascular smooth muscle cells.Acta pharmacologica Sinica · 2018Article
- Essential role of SH3GL1 in interleukin-6(IL-6)- and vascular endothelial growth factor (VEGF)-triggered p130Human cell · 2017Article
- ClC-3 Chloride Channel Proteins Regulate the Cell Cycle by Up-regulating cyclin D1-CDK4/6 through Suppressing p21/p27 Expression in Nasopharyngeal Carcinoma Cells.Scientific reports · 2016Article
- Threonine532 phosphorylation in ClC-3 channels is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells.British journal of pharmacology · 2016Article
- ClC-3 chloride channel modulates the proliferation and migration of osteosarcoma cells via AKT/GSK3β signaling pathway.International journal of clinical and experimental pathology · 2015Article
- Integrin β3 mediates cerebrovascular remodelling through Src/ClC-3 volume-regulated Cl(-) channel signalling pathway.British journal of pharmacology · 2014Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Chloride channels in stroke.Acta pharmacologica Sinica · 2013Review
- Cell cycle-dependent subcellular distribution of ClC-3 in HeLa cells.Histochemistry and cell biology · 2012Article
- The MSX1 homeoprotein recruits G9a methyltransferase to repressed target genes in myoblast cells.PloS one · 2012Article
- Ano1 as a regulator of proliferation.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- The ClC-3 chloride channels in cardiovascular disease.Acta pharmacologica Sinica · 2011Review
- Endosomal ClC-3 and Nox1: moving marksmen of redox signaling?Arteriosclerosis, thrombosis, and vascular biology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPreviously, we have found that the ClC-3 chloride channel is involved in endothelin-1 (ET-1)-induced rat aortic smooth muscle cell proliferation. The present study was to investigate the role of ClC-3 in cell cycle progression/distribution and the underlying mechanisms of proliferation. MATERIALS AND
methodsSmall interference RNA (siRNA) is used to silence ClC-3 expression. Cell proliferation, cell cycle distribution and protein expression were measured or detected with cell counting, bromodeoxyuridine (BrdU) incorporation, Western blot and flow cytometric assays respectively.
resultsET-1-induced rat basilar vascular smooth muscle cell (BASMC) proliferation was parallel to a significant increase in endogenous expression of ClC-3 protein. Silence of ClC-3 by siRNA inhibited expression of ClC-3 protein, prevented an increase in BrdU incorporation and cell number induced by ET-1. Silence of ClC-3 also caused cell cycle arrest in G(0)/G(1) phase and prevented the cells' progression from G(1) to S phase. Knockdown of ClC-3 potently inhibited cyclin D1 and cyclin E expression and increased cyclin-dependent kinase inhibitors (CDKIs) p27(KIP) and p21(CIP) expression. Furthermore, ClC-3 knockdown significantly attenuated phosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta) induced by ET-1.
conclusionSilence of ClC-3 protein effectively suppressed phosphorylation of the Akt/GSK-3beta signal pathway, resulting in down-regulation of cyclin D1 and cyclin E, and up-regulation of p27(KIP) and p21(CIP). In these BASMCs, integrated effects lead to cell cycle G(1)/S arrest and inhibition of cell proliferation.
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