<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kim HP</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>11319-24</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1183544</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>102(32)</volume><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</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide.</pubmed_title><pmcid>PMC1183544</pmcid><funding_grant_id>R01 HL060234</funding_grant_id><funding_grant_id>R01-HL55330</funding_grant_id><funding_grant_id>R01-AI42365</funding_grant_id><funding_grant_id>R01-HL60234</funding_grant_id><funding_grant_id>R01 HL055330</funding_grant_id><pubmed_authors>Kim SI</pubmed_authors><pubmed_authors>Ryter SW</pubmed_authors><pubmed_authors>Choi AM</pubmed_authors><pubmed_authors>Nakao A</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Kim HP</pubmed_authors><pubmed_authors>Choi ME</pubmed_authors><pubmed_authors>Murase N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide.</name><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</description><dates><release>2005-01-01T00:00:00Z</release><publication>2005 Aug</publication><modification>2026-05-30T02:34:48.958Z</modification><creation>2019-03-27T01:09:14Z</creation></dates><accession>S-EPMC1183544</accession><cross_references><pubmed>16051704</pubmed><doi>10.1073/pnas.0501345102</doi></cross_references></HashMap>