{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee GS"],"funding":["NHLBI NIH HHS","U.S. Department of Health &amp; Human Services | NIH | National Heart, Lung, and Blood Institute"],"pagination":["331-345"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6311150"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["99(3)"],"pubmed_abstract":["Osteopontin (OPN) is critical for ischemia-induced neovascularization. Unlike rodents, humans express three OPN isoforms (a, b, and c); however, the roles of these isoforms in post-ischemic neovascularization and cell migration remain undefined. Our objective was to determine if OPN isoforms differentially affect post-ischemic neovascularization and to elucidate the mechanisms underlying these differences. To investigate if human OPN isoforms exert divergent effects on post-ischemic neovascularization, we utilized OPN<sup>-/-</sup> mice and a loss-of-function/gain-of-function approach in vivo and in vitro. In this study OPN<sup>-/-</sup> mice underwent hindlimb ischemia surgery and 1.5 × 10<sup>6</sup> lentivirus particles were administered intramuscularly to overexpress OPNa, OPNb, or OPN"],"journal":["Laboratory investigation; a journal of technical methods and pathology"],"pubmed_title":["Osteopontin isoforms differentially promote arteriogenesis in response to ischemia via macrophage accumulation and survival."],"pmcid":["PMC6311150"],"funding_grant_id":["F32 HL137401","P01 HL095070","F32HL137401","T32 HL007745","R00HL119567","P01HL095070","R00 HL119567","K99 HL119567","5T32HL007745-24"],"pubmed_authors":["Lyle AN","Caroti CM","Salazar HF","Weiss D","Taylor WR","Lee GS","Joseph G","Lok ZSY"],"additional_accession":[]},"is_claimable":false,"name":"Osteopontin isoforms differentially promote arteriogenesis in response to ischemia via macrophage accumulation and survival.","description":"Osteopontin (OPN) is critical for ischemia-induced neovascularization. Unlike rodents, humans express three OPN isoforms (a, b, and c); however, the roles of these isoforms in post-ischemic neovascularization and cell migration remain undefined. Our objective was to determine if OPN isoforms differentially affect post-ischemic neovascularization and to elucidate the mechanisms underlying these differences. To investigate if human OPN isoforms exert divergent effects on post-ischemic neovascularization, we utilized OPN<sup>-/-</sup> mice and a loss-of-function/gain-of-function approach in vivo and in vitro. In this study OPN<sup>-/-</sup> mice underwent hindlimb ischemia surgery and 1.5 × 10<sup>6</sup> lentivirus particles were administered intramuscularly to overexpress OPNa, OPNb, or OPN","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Mar","modification":"2025-04-19T22:51:12.02Z","creation":"2019-03-26T22:27:51Z"},"accession":"S-EPMC6311150","cross_references":{"pubmed":["29959420"],"doi":["10.1038/s41374-018-0094-8"]}}