| First Author | Rivera LB | Year | 2011 |
| Journal | J Cell Biol | Volume | 193 |
| Issue | 7 | Pages | 1305-19 |
| PubMed ID | 21708981 | Mgi Jnum | J:174202 |
| Mgi Id | MGI:5052198 | Doi | 10.1083/jcb.201011143 |
| Citation | Rivera LB, et al. (2011) SPARC promotes pericyte recruitment via inhibition of endoglin-dependent TGF-{beta}1 activity. J Cell Biol 193(7):1305-19 |
| abstractText | Pericytes migrate to nascent vessels and promote vessel stability. Recently, we reported that secreted protein acidic and rich in cysteine (SPARC)-deficient mice exhibited decreased pericyte-associated vessels in an orthotopic model of pancreatic cancer, suggesting that SPARC influences pericyte behavior. In this paper, we report that SPARC promotes pericyte migration by regulating the function of endoglin, a TGF-beta1 accessory receptor. Primary SPARC-deficient pericytes exhibited increased basal TGF-beta1 activity and decreased cell migration, an effect blocked by inhibiting TGF-beta1. Furthermore, TGF-beta-mediated inhibition of pericyte migration was dependent on endoglin and alphaV integrin. SPARC interacted directly with endoglin and reduced endoglin interaction with alphaV integrin. SPARC deficiency resulted in endoglin-mediated blockade of pericyte migration, aberrant association of endoglin in focal complexes, an increase in alphaV integrins present in endoglin immunoprecipitates, and enhanced alphaV integrin-mediated activation of TGF-beta. These results demonstrate that SPARC promotes pericyte migration by diminishing TGF-beta activity and identify a novel function for endoglin in controlling pericyte behavior. |
