J. Biol. Chem., Vol. 283, Issue 31, 21305-21309, August 1, 2008
Current Position: Professor of Pharmacology at the Institute for General Pharmacology and Toxicology at Goethe-University in Frankfurt, Germany
Education: M.D. (1992) from the University of Wuerzburg in Germany
Non-scientific Interests: Architecture, arts, travel, and family
As a physician, I was first trained in Nephrology and further focused my research on understanding the mechanisms that lead to renal fibrosis. In the mid-1990s, the small leucine-rich proteoglycan decorin was shown to bind and inactivate TGF-β and was subsequently touted as a promising anti-fibrotic agent. This biological property was soon found to be shared by other SLRPs such as biglycan. However, biglycan, in contrast to decorin, evokes pro-inflammatory rather than anti-fibrotic effects. Following renal injury, biglycan is frequently expressed by tubular epithelial cells and acts as a recruiting signal for infiltrating macrophages. By further analyzing this macrophage response, we found that biglycan acts as an endogenous ligand for Toll-like receptor-2 and -4 on macrophages, giving rise to the concept that, under certain conditions, matrix components may act as endogenous “danger” signals, which can be recognized by innate immunity receptors.
Read Dr. Schaefer's article on page 21305.
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