1. ¹Dermatology Service, Palo Alto VA Health Care System, Stanford University School of Medicine, Stanford, California, USA
2. ²Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA

Correspondence: Professor M. Peter Marinkovich, Program in Epithelial Biology, Stanford University School of Medicine, 269 Campus Drive, Room 2145, Stanford, California 94305, USA. E-mail: mpm@stanford.edu

³Current address: Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Florida 33136, USA

Received 9 December 2004; Revised 15 September 2005; Accepted 22 September 2005; Published online 22 December 2005.

Abstract

This study examined the effects of endogenous overexpression of laminin-8 on angiogenesis and wound healing in primary human dermal microvascular endothelial cells (HDMECs). HDMECs expressed laminin-8 and laminin-10, but no other laminins, as determined by radioimmunoprecipitation assay using a panel of antibodies to individual laminin chains. To study laminin-8 function, full-length human laminin 4 cDNA was retrovirally transferred to HDMEC, and specific overexpression of laminin-8 was verified by Western blot. Laminin-8 overexpression promoted endothelial cell spreading and migration in scratch assays and accelerated angiogenic tubule formation in collagen gel overlay assays. Strong inhibitory effect of 1 integrin and weak inhibition by v3 integrin antibodies were observed in laminin-8-stimulated cell migration, but only 1 integrin antibodies affected tubule formation. These studies suggest that laminin-8 overexpression may prove to be a useful method to engineer HDMECs to promote angiogenesis and wound repair.