Laminin-511 and integrin beta-1 in hair follicle development and basal cell carcinoma formation
1 Cancer Biology Graduate Program 251 Campus Drive, MSOB X234, Stanford, 94305-5173), USA
2 Program in Epithelial Biology, Stanford University, School of Medicine, CCSR 2145c, 269 Campus Drive, Stanford, CA 94305, USA
3 Dermatology Service, Palo Alto VA Medical Center, 3801 Miranda Ave Palo Alto, California 94304, USA
BMC Developmental Biology 2010, 10:112 doi:10.1186/1471-213X-10-112Published: 10 November 2010
Initiation of the hair follicle placode and its subsequent growth, maturation and cycling in post-natal skin requires signaling interactions between epithelial cells and adjacent dermal cells and involves Shh signaling via the primary cilium. Previous reports have implicated laminins in hair follicle epithelial invagination.
Here we use a human BCC model system and mouse mutants to re-evaluate the role of laminin-511 in epithelial invagination in the skin. Blocking laminin 511 and 332 in BCCs maintains primary cilia and Shh signalling, but prevents invagination. Similarly, in laminin-511 and dermal beta-1 integrin mutants, dermal papilla development and primary cilia formation are normal. Dermal beta-1 integrin mutants have normal hair follicle development.
Our data provides support for a primary role of laminin-511 promoting hair follicle epithelial downgrowth without affecting dermal primary cilia and Shh target gene induction.