Dexamethasone resisted podocyte injury

Abstract

CD2AP and TRPC6, the key proteins of podocyte slit diaphragm (SD), together form a signal transduction complex by interacting with other SD molecules and also play an important role in maintaining SD structural and functional integrity. Data suggest that podocyte injury or SD structural damage will inevitably result in proteinuria. Proteinuria is a hallmark of loss of the glomerulus’ permselectivity. In many cases, persistent dysfunction of the glomerular filtration barrier leads to progressive renal failure. Together, glomerular proteinuria represents a major cause of renal failure and need for dialysis or kidney transplantation. In this study, we investigated whether and how the puromycin aminonucleoside (PAN) induced podocyte injury and dexamethasone (DEX) repaired podocyte. We explored the expression and distribution changes of CD2AP and TRPC6. These findings emphasized the important roles of CD2AP and TRPC6 in podocyte. These results also implicate that DEX repaired different degrees of podocyte injury, which might have resulted from different molecular mechanisms. Our findings provide some possible clues for further exploring the pharmacological targets to the proteinuria.

Key words: Dexamethasone, podocyte, slit diaphragm, CD2AP, TRPC6.