Osteopontin isoforms differentially promote arteriogenesis in response to ischemia via macrophage accumulation and survival.

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^-/- mice and a loss-of-function/gain-of-function approach in vivo and in vitro. In this study OPN^-/- mice underwent hindlimb ischemia surgery and 1.5 × 10⁶ lentivirus particles were administered intramuscularly to overexpress OPNa, OPNb, or OPN

SUBMITTER: Lee GS 

PROVIDER: S-EPMC6311150 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature