ArticleBritish journal of pharmacology2005
ClC-3 chloride channel is upregulated by hypertrophy and inflammation in rat and canine pulmonary artery.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 68 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Structural basis of adenine nucleotides regulation and neurodegenerative pathology in ClC-3 exchanger.Nature communications · 2024Article
- ANO1, CaV1.2, and IP3R form a localized unit of EC-coupling in mouse pulmonary arterial smooth muscle.The Journal of general physiology · 2023Article
- Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels.The Journal of membrane biology · 2023Article
- MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM.Journal of translational medicine · 2018Article
- Betaine Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibiting Inflammatory Response.Molecules (Basel, Switzerland) · 2018Article
- The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- 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
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Increased TMEM16A-encoded calcium-activated chloride channel activity is associated with pulmonary hypertension.American journal of physiology. Cell physiology · 2012Article
- Chronic hypoxia-induced upregulation of Ca2+-activated Cl- channel in pulmonary arterial myocytes: a mechanism contributing to enhanced vasoreactivity.The Journal of physiology · 2012Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Endothelial and smooth muscle cell ion channels in pulmonary vasoconstriction and vascular remodeling.Comprehensive Physiology · 2011Review
- 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
- A critical role for chloride channel-3 (CIC-3) in smooth muscle cell activation and neointima formation.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- Activation of swelling-activated chloride current by tumor necrosis factor-alpha requires ClC-3-dependent endosomal reactive oxygen production.The Journal of biological chemistry · 2010Article
- Expression of chloride channels in trachea-occluded hyperplastic lungs and nitrofen-induced hypoplastic lungs in rats.Pediatric surgery international · 2009Article
- TRPC1 and STIM1 mediate capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells.The Journal of physiology · 2009Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
Cl- channels have been implicated in essential cellular functions including volume regulation, progression of cell cycle, cell proliferation and contraction, but the physiological functions of the ClC-3 channel are controversial. We tested the hypothesis that the ClC-3 gene (ClCn-3) is upregulated in hypertensive pulmonary arteries of monocrotaline-treated rats, and upregulated ClC-3 channel aids viability of pulmonary artery smooth muscle cells (PASMCs). Experimental pulmonary hypertension was induced in rats by a single subcutaneous administration of monocrotaline (60 mg kg(-1)). Injected animals developed characteristic features of pulmonary hypertension including medial hypertrophy of pulmonary arteries and right ventricular hypertrophy. Reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry and Western immunoblot analysis indicated that histopathological alterations were associated with upregulation of the ClC-3 mRNA and protein expression in both smooth muscle cells of hypertensive pulmonary arteries and in cardiac myocytes. RT-PCR analysis of mRNA, extracted from canine cultured PASMCs, indicated that incubation with the inflammatory mediators endothelin-1 (ET-1), platelet-derived growth factor (PDGF), interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF alpha), but not transforming growth factor beta (TGFbeta), upregulated ClC-3 mRNA. Adenovirus-mediated delivery and overexpression of ClC-3 in canine PASMCs improved cell viability against increasing concentrations of hydrogen peroxide (H2O2, range 50-250 microM). In conclusion, upregulation of ClC-3 in rat hypertensive lung and heart is a novel observation. Our functional data suggest that upregulation of ClC-3 is an adaptive response of inflamed pulmonary artery, which enhances the viability of PASMCs against reactive oxygen species.
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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.