ArticleArteriosclerosis, thrombosis, and vascular biology2011
A critical role for chloride channel-3 (CIC-3) in smooth muscle cell activation and neointima formation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels.The Journal of membrane biology · 2023Article
- Reduced intracellular chloride concentration impairs angiogenesis by inhibiting oxidative stress-mediated VEGFR2 activation.Acta pharmacologica Sinica · 2021Article
- NOXA1-dependent NADPH oxidase regulates redox signaling and phenotype of vascular smooth muscle cell during atherogenesis.Redox biology · 2019Article
- ClC-3 promotes angiotensin II-induced reactive oxygen species production in endothelial cells by facilitating Nox2 NADPH oxidase complex formation.Acta pharmacologica Sinica · 2018Article
- NOX2 oxidase expressed in endosomes promotes cell proliferation and prostate tumour development.Oncotarget · 2018Article
- Endothelial Nox1 oxidase assembly in human pulmonary arterial hypertension; driver of Gremlin1-mediated proliferation.Clinical science (London, England : 1979) · 2017Article
- LRRC8A channels support TNFα-induced superoxide production by Nox1 which is required for receptor endocytosis.Free radical biology & medicine · 2016Article
- 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
- ClC-3 Expression and Its Association with Hyperglycemia Induced HT22 Hippocampal Neuronal Cell Apoptosis.Journal of diabetes research · 2016Article
- Hypoxia-dependent reactive oxygen species signaling in the pulmonary circulation: focus on ion channels.Antioxidants & redox signaling · 2015Review
- Novel CLC3 transcript variants in blood eosinophils and increased CLC3 expression in nasal lavage and blood eosinophils of asthmatics.Immunity, inflammation and disease · 2014Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Increase in hypotonic stress-induced endocytic activity in macrophages via ClC-3.Molecules and cells · 2014Article
- The basic biology of redoxosomes in cytokine-mediated signal transduction and implications for disease-specific therapies.Biochemistry · 2014Review
- ClC-3 chloride channel in hippocampal neuronal apoptosis.Neural regeneration research · 2013Article
- Chloride channels in stroke.Acta pharmacologica Sinica · 2013Review
- Functional regulation of ClC-3 in the migration of vascular smooth muscle cells.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system.Circulation research · 2012Review
- Differential roles of NADPH oxidases in vascular physiology and pathophysiology.Frontiers in bioscience (Scholar edition) · 2012Review
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8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe have shown that the chloride-proton antiporter chloride channel-3 (ClC-3) is required for endosome-dependent signaling by the Nox1 NADPH oxidase in SMCs. In this study, we tested the hypothesis that ClC-3 is necessary for proliferation of smooth muscle cells (SMCs) and contributes to neointimal hyperplasia following vascular injury. METHODS AND
resultsStudies were performed in SMCs isolated from the aorta of ClC-3-null and littermate control (wild-type [WT]) mice. Thrombin and tumor necrosis factor-α (TNF-α) each caused activation of both mitogen activated protein kinase extracellular signal-regulated kinases 1 and 2 and the matrix-degrading enzyme matrix metalloproteinase-9 and cell proliferation of WT SMCs. Whereas responses to thrombin were preserved in ClC-3-null SMCs, the responses to TNF-α were markedly impaired. These defects normalized following gene transfer of ClC-3. Carotid injury increased vascular ClC-3 expression, and compared with WT mice, ClC-3-null mice exhibited a reduction in neointimal area of the carotid artery 28 days after injury.
conclusionsClC-3 is necessary for the activation of SMCs by TNF-α but not thrombin. Deficiency of ClC-3 markedly reduces neointimal hyperplasia following vascular injury. In view of our previous findings, this observation is consistent with a role for ClC-3 in endosomal Nox1-dependent signaling. These findings identify ClC-3 as a novel target for the prevention of inflammatory and proliferative vascular diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.