Endothelial-fibroblastic cell interactions in fibrosis

Organ fibrosis contributes to the top 10 causes of death in Canada, affects >6.5M North Americans, consumes >$25 billion in global healthcare expenses, and is a major burden for patients, families, and our society. One of the main signals driving fibrosis is persistent and excessive production of the growth factor TGF-beta. The Hinz lab identified vascular endothelial cells as a major and yet poorly characterized source of TGF-beta. We propose that, in response to injury and inflammation, endothelial cells ‘hand-over’ active TGF-beta to closely associated perivascular ‘fibroblasts’. Stimulated by TGF-beta, perivascular fibroblasts continuously secrete and contract collagen matrix into stiff fibrotic scar. This undergraduate project aims at deciphering the mechanisms of TGF-beta presentation by endothelial cells and reception by fibroblasts in the perivascular niche to reveal new potential targets for anti-fibrosis therapies.

Faculty Supervisor:

Boris Hinz

Student:

Partner:

Reutlingen University

Discipline:

Life Sciences

Sector:

Education

University:

University of Toronto

Program: