{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim HP"],"funding":["NIAID NIH HHS","NHLBI NIH HHS"],"pagination":["11319-24"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1183544"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["102(32)"],"pubmed_abstract":["During vascular injury, the proliferation and migration of smooth muscle cells leads to characteristic neointima formation, which can be exacerbated by genetic depletion of caveolin-1 or heme oxygenase 1 (HO-1), and inhibited by carbon monoxide (CO), a by-product of heme oxygenase 1 activity. CO inhibited smooth muscle cell proliferation by activating p38 mitogen-activated protein kinase (MAPK) and p21(Waf1/Cip1). Exposure to CO increased caveolin-1 expression in neointimal lesions of injured aorta and in vitro by activating guanylyl cyclase and p38 MAPK. p38beta-/- fibroblasts did not induce caveolin-1 in response to CO, and exhibited a diminished basal caveolin-1 expression, which was restored by p38beta gene transfer. p38beta MAPK down-regulated extracellular signal-regulated protein ki"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide."],"pmcid":["PMC1183544"],"funding_grant_id":["R01 HL060234","R01-HL55330","R01-AI42365","R01-HL60234","R01 HL055330"],"pubmed_authors":["Kim SI","Ryter SW","Choi AM","Nakao A","Wang X","Kim HP","Choi ME","Murase N"],"additional_accession":[]},"is_claimable":false,"name":"Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide.","description":"During vascular injury, the proliferation and migration of smooth muscle cells leads to characteristic neointima formation, which can be exacerbated by genetic depletion of caveolin-1 or heme oxygenase 1 (HO-1), and inhibited by carbon monoxide (CO), a by-product of heme oxygenase 1 activity. CO inhibited smooth muscle cell proliferation by activating p38 mitogen-activated protein kinase (MAPK) and p21(Waf1/Cip1). Exposure to CO increased caveolin-1 expression in neointimal lesions of injured aorta and in vitro by activating guanylyl cyclase and p38 MAPK. p38beta-/- fibroblasts did not induce caveolin-1 in response to CO, and exhibited a diminished basal caveolin-1 expression, which was restored by p38beta gene transfer. p38beta MAPK down-regulated extracellular signal-regulated protein ki","dates":{"release":"2005-01-01T00:00:00Z","publication":"2005 Aug","modification":"2026-05-30T02:34:48.958Z","creation":"2019-03-27T01:09:14Z"},"accession":"S-EPMC1183544","cross_references":{"pubmed":["16051704"],"doi":["10.1073/pnas.0501345102"]}}