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Plastic Surgery Research laboratory (Philip Lab)

Research in our laboratory focuses on understanding the role of TGF-b signaling in wound healing, scarring and fibrosis in the skin, and in regulating chondrocyte phenotype and function in healthy and diseased cartilage. The work on TGF-b signaling in skin focuses on TGF-b co-receptors as regulators of TGF-b signaling in human skin cells. Recently, we have shown that CD109, a TGF-b co-receptor inhibits TGF-b signaling by promoting caveolar compartmentalization of TGF-b signaling receptors leading to their degradation and termination of signaling.  Furthermore, transgenic mice that overexpress CD109 in the epidermis display improved wound healing, reduced scarring and a resistance to fibrosis in a mouse model of scleroderma. Our current research involves the development of novel TGF-b antagonists and anti-fibrotic agents for the treatment of pathological conditions including hypertrophic scarring and scleroderma.

Our research on human cartilage cells (chondrocytes) centers on understanding the functional interplay between a novel TGF-b signaling receptor (activin receptor-like kinase 1, or ALK1) and the co-receptor endoglin  in regulating chondrocyte phenotype and function in healthy and osteoarthritic cartilage. We have shown that ALK1 and endoglin interact in human chondrocytes to attenuate TGF-b signaling via the 'canonical' TGF-b/ALK5 signaling pathway leading to decreased production of type II collagen and aggrecan which play essential roles in the maintenance of healthy cartilage. Our current research in this area focuses on characterizing the functional role of ALK1 and endoglin in experimental models of osteoarthritis. The work in our laboratory is supported by Canadian Institute for Health Research (CIHR), Natural Sciences and Engineering Research Council (NSERC) and the United States Department of Defence (DOD).