{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Duggirala A"],"funding":["British Heart Foundation","NIHR Bristol BRU in Cardiovascular Medicine"],"pagination":["157-68"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4312355"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["79"],"pubmed_abstract":["Elevation of intracellular cAMP concentration has numerous vascular protective effects that are in part mediated via actin cytoskeleton-remodelling and subsequent regulation of gene expression. However, the mechanisms are incompletely understood. Here we investigated whether cAMP-induced actin-cytoskeleton remodelling modulates VSMC behaviour by inhibiting expression of CCN1. In cultured rat VSMC, CCN1-silencing significantly inhibited BrdU incorporation and migration in a wound healing assay. Recombinant CCN1 enhanced chemotaxis in a Boyden chamber. Adding db-cAMP, or elevating cAMP using forskolin, significantly inhibited CCN1 mRNA and protein expression in vitro; transcriptional regulation was demonstrated by measuring pre-spliced CCN1 mRNA and CCN1-promoter activity. Forskolin also inh"],"journal":["Journal of molecular and cellular cardiology"],"pubmed_title":["cAMP-induced actin cytoskeleton remodelling inhibits MKL1-dependent expression of the chemotactic and pro-proliferative factor, CCN1."],"pmcid":["PMC4312355"],"funding_grant_id":["PG/11/78/29113"],"pubmed_authors":["Sala-Newby GB","Johnson JL","Kimura TE","Newby AC","Wu YJ","Duggirala A","Bond M"],"additional_accession":[]},"is_claimable":false,"name":"cAMP-induced actin cytoskeleton remodelling inhibits MKL1-dependent expression of the chemotactic and pro-proliferative factor, CCN1.","description":"Elevation of intracellular cAMP concentration has numerous vascular protective effects that are in part mediated via actin cytoskeleton-remodelling and subsequent regulation of gene expression. However, the mechanisms are incompletely understood. Here we investigated whether cAMP-induced actin-cytoskeleton remodelling modulates VSMC behaviour by inhibiting expression of CCN1. In cultured rat VSMC, CCN1-silencing significantly inhibited BrdU incorporation and migration in a wound healing assay. Recombinant CCN1 enhanced chemotaxis in a Boyden chamber. Adding db-cAMP, or elevating cAMP using forskolin, significantly inhibited CCN1 mRNA and protein expression in vitro; transcriptional regulation was demonstrated by measuring pre-spliced CCN1 mRNA and CCN1-promoter activity. Forskolin also inh","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Feb","modification":"2025-04-19T14:40:46.548Z","creation":"2019-03-27T01:44:21Z"},"accession":"S-EPMC4312355","cross_references":{"pubmed":["25446180"],"doi":["10.1016/j.yjmcc.2014.11.012"]}}