ArticleCardiovascular research2007
Involvement of chloride channels in IGF-I-induced proliferation of porcine arterial smooth muscle cells.
Article in Cardiovascular research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 34 citations in OpenAlex.
- An All-Optical Approach to Probe Chloride Transport with a Bright ChlorON.bioRxiv : the preprint server for biology · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- CircRNACells · 2026Article
- The Role of Ion Channels in Pulmonary Hypertension: A Review.Pulmonary circulation · 2025Review
- Two Different Copy Number Variations of theAnimals : an open access journal from MDPI · 2021Article
- Inhibition of angiotensin II-induced cerebrovascular smooth muscle cell proliferation by LRRC8A downregulation through suppressing PI3K/AKT activation.Human cell · 2019Article
- ClC-2 knockdown prevents cerebrovascular remodeling via inhibition of the Wnt/β-catenin signaling pathway.Cellular & molecular biology letters · 2018Article
- Cellular functions of TMEM16/anoctamin.Pflugers Archiv : European journal of physiology · 2016Review
- The rs3737964 single-nucleotide polymorphism of the chloride channel-6 gene as a risk factor for coronary heart disease.Molecular genetics & genomic medicine · 2015Article
- Requirement for chloride channel function during the hepatitis C virus life cycle.Journal of virology · 2015Article
- The hidden hand of chloride in hypertension.Pflugers Archiv : European journal of physiology · 2015Review
- Current siRNA targets in the prevention and treatment of intimal hyperplasia.Discovery medicine · 2014Review
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Chloride channelopathies of ClC-2.International journal of molecular sciences · 2013Review
- An angiotensin II- and NF-kappaB-dependent mechanism increases connexin 43 in murine arteries targeted by renin-dependent hypertension.Cardiovascular research · 2010Article
- CBP knockdown inhibits angiotensin II-induced vascular smooth muscle cells proliferation through downregulating NF-kB transcriptional activity.Molecular and cellular biochemistry · 2010Article
- Isolation and characterization of a high affinity peptide inhibitor of ClC-2 chloride channels.The Journal of biological chemistry · 2009Article
- Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway.Journal of molecular and cellular cardiology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe existence of Cl- channels in vascular smooth muscle cells (VSMCs) has been increasingly investigated, but the biological functions are not yet clear. Insulin-like growth factor (IGF)-I affects proliferation and migration of VSMCs, and dysregulation of this axis may be involved in atherogenesis and intimal hyperplasia. We examined the effects of Cl- channel blockers on IGF-I-induced proliferation in porcine VSMCs. The siRNA approach was used to support the role of ClC-2, a member of the volume-regulated Cl- channel family, in cell proliferation of VSMCs. METHODS AND
resultsThe IGF-I-induced VSMC proliferation was significantly suppressed by the Cl- channel blockers NPPB and IAA94 but not by DIDS. IGF-I-induced cell proliferation parallels a significant increase in the endogenous expression of ClC-2 mRNA and protein. Inhibitors of PI3-kinase, LY294002 and wortmannin, significantly attenuated the IGF-I-upregulated ClC-2 expression and cell proliferation. We observed ClC-2-like Cl- current, and this current was augmented by IGF-I. SiRNA specifically targeted to ClC-2 abolished IGF-I-induced cell proliferation.
conclusionOur data demonstrate that ClC-2 plays a role in IGF-1-induced regulation of VSMC proliferation in cardiovascular diseases.
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Registered trials
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.