{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liao S"],"funding":["NHLBI NIH HHS"],"pagination":["106-20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1852491"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(1)"],"pubmed_abstract":["<h4>Unlabelled</h4>Our laboratory showed that overexpression of fibroblast growth factor-2 (FGF2) protected the heart against ischemia-reperfusion injury. FGF2 has different protein isoforms (low [LMW] and high [HMW] molecular weight isoforms) produced from alternative translation start sites. However, which FGF2 isoform(s) mediates this cardioprotection, and which signaling pathway (i.e., mitogen-activated protein kinase (MAPK)) elicits FGF2 isoform-induced cardioprotection remains to be elucidated.<h4>Methods and results</h4>Wildtype, Fgf2 KO (absence of all FGF2 isoforms) and FGF2 LMWKO (absence of LMW isoform) hearts were subjected to an ex vivo work-performing heart ischemic model of 60 min ischemia and 120 min reperfusion. There was a significant decrease in the recovery of post-isch"],"journal":["Journal of molecular and cellular cardiology"],"pubmed_title":["The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling."],"pmcid":["PMC1852491"],"funding_grant_id":["R01 HL075633","R56 HL075633","R01 HL070174"],"pubmed_authors":["Schultz Jel J","Scott A","Liao S","Doetschman T","Porter D","Newman G"],"additional_accession":[]},"is_claimable":false,"name":"The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling.","description":"<h4>Unlabelled</h4>Our laboratory showed that overexpression of fibroblast growth factor-2 (FGF2) protected the heart against ischemia-reperfusion injury. FGF2 has different protein isoforms (low [LMW] and high [HMW] molecular weight isoforms) produced from alternative translation start sites. However, which FGF2 isoform(s) mediates this cardioprotection, and which signaling pathway (i.e., mitogen-activated protein kinase (MAPK)) elicits FGF2 isoform-induced cardioprotection remains to be elucidated.<h4>Methods and results</h4>Wildtype, Fgf2 KO (absence of all FGF2 isoforms) and FGF2 LMWKO (absence of LMW isoform) hearts were subjected to an ex vivo work-performing heart ischemic model of 60 min ischemia and 120 min reperfusion. There was a significant decrease in the recovery of post-isch","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Jan","modification":"2025-04-04T07:10:29.767Z","creation":"2019-06-06T14:03:40Z"},"accession":"S-EPMC1852491","cross_references":{"pubmed":["17150229"],"doi":["10.1016/j.yjmcc.2006.10.005"]}}