Open AccessBone morphogenetic protein-7 delays podocyte injury due to high glucose
Author(s) -
Laura De Petris,
Keith A. Hruska,
Santina Chiechio,
Helen Liapis
Publication year - 2007
Publication title -
nephrology, dialysis, transplantation/nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfm503
Subject(s) - synaptopodin , podocin , podocyte , bone morphogenetic protein , bone morphogenetic protein 7 , endocrinology , medicine , microbiology and biotechnology , biology , biochemistry , kidney , gene , proteinuria
The molecular pathogenesis of diabetic glomerulosclerosis remains unknown, but recent studies suggest that podocyte damage may play a role. Bone morphogenetic protein 7 (BMP-7) is physiologically expressed in podocytes and tubular epithelial cells. Our previous studies show that BMP-7 reverses glomerular and tubulointerstitial damage in diabetic rats, but there is little known about possible effects of BMP-7 on podocytes. We postulate that high glucose may injure the podocyte by altering structural proteins such as synaptopodin and podocin. This study investigates the effect of high glucose on mouse podocytes, expression of synaptopodin and podocin under normal and high glucose and the treatment effect of BMP-7 on these molecules. Human diabetic glomeruli are studied in parallel.