The plant pathogenesis related protein GLIPR-2 is highly expressed in fibrotic kidney and promotes epithelial to mesenchymal transition in vitro.

Fibrosis is the accumulation of extracellular matrix proteins and is a common end pathway in many chronic diseases. To identify novel mediators of fibrosis we used transcript profiling in a mouse model of kidney fibrosis, the COL4A3 knockout (alport) mouse. One gene that we found up-regulated in fibrotic kidney was GLIPR-2, also known as GAPR-1 and C9orf19, a member of the plant pathogenesis-related proteins family 1. We have found that GLIPR-2 protein expression is significantly increased in fibrotic kidney compared to healthy controls. Examination of the expression pattern of GLIPR-2 indicated that the protein is selectively expressed in epithelial cells. Co-staining with antibodies for alpha-smooth muscle actin expression, a marker of myofibroblasts, showed that GLIPR-2 expressing cells are closely apposed to areas of strong alpha-smooth muscle actin expression. The origin of these myofibroblasts is not known, but in vitro studies have shown that GLIPR-2 can induce epithelial to mesenchymal transition (EMT) in a renal epithelial cell line. We propose that increased GLIPR-2 expression in kidney contributes to development of fibrosis by increasing the pool of activated fibroblasts, possibly through the induction of EMT.

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