Anie Philip

Anie Philip

Title:

Professor, Department of Surgery
Associate Member, Department of Medicine, Division of Experimental Medicine

Area of Research: Skin and Cartilage repair

Contact Information:

anie.philip [at] mcgill.ca (Email)

Tel: 514-934-1934, ext. 44533

Lab Website

Recents Publications:

Publications indexed to PubMed

 

Current research: 

Fibrosis, Scarring, Wound Healing, Cancer Metastasis

Summary of Work:

Impaired wound healing of the skin and defective repair of the articular cartilage are major medical problems, with limited treatment options. Growth factors are acknowledged to play critical roles in tissue repair events. Of the many growth factors, transforming growth factor-beta (TGF-beta) is remarkable in its potential to influence almost all aspects of tissue repair. The therapeutic potential of exogenous TGF-beta to promote wound healing in the skin and enhance cartilage repair is well documented in animal models. However, clinical results in humans have been discouraging, possible due to inappropriate timing of administration and unavailability of the delivered factor. An alternative approach would be to manipulate the action of endogenous TGF-beta locally using regulatory molecules. Identification of such modulators will provide a novel avenue for therapeutic manipulation of TGF-beta action to regulate the repair process. TGF-beta action is most likely to be regulated at the level of its bioavailability, receptors and signaling. Thus, our research program is focused on identifying factors that may regulate these parameters in skin and cartilage cells, specifically, keratinocytes, endothelial cells and chondrocytes.

Recent results from our laboratory suggest that such factors include steroids, oxygen tension, and novel cell surface TGF-beta binding proteins. Significantly, we identified and cloned a novel TGF-beta receptor, r150, which interacts with the TGF-beta signaling receptors and inhibits signaling in human keratinocytes. On chondrocytes, we demonstrated the expression and function of TGF-beta receptors previously not known to e present on hese cells. Steroids and oxygen tension have profound effects on tissue repair, and our results suggest that these agents may exert their effects, at least in part, by modulating TGF-beta action.

The on-going projects in our laboratory are driven by the following three hypotheses: (1) That novel cell surface TGF-beta binding proteins expressed on human skin and cartilage cells modulate TGF-beta signaling, and therefore cana be used for the development of agents that regulate TGF-beta action, and thus promote repair; (2) That steroids and oxygen tension regulate TGF-beta bioavailability and TGF-beta receptors in skin and cartilage cells, and as such can be used to manipuplate TGF-beta action, and thus repair; (3) That skin and cartilage cells display age and/or phenotype dependent regulation of TGF-beta action, and such differential regulation is responsible for the age/phenotype associated impairment of wound repair.

The work in our laboratory is supported by Canadian Institute for Health Research, Heart and Stroke Foundation, Quebec and FRSQ.

 

 

 

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