PC 1 NF suppresses high glucose stimulated inflammation and extracellular matrix accumulation in glomerular mesangial cells via the Wnt/b catenin signaling
Diabetic nephropathy (DN) is the leading cause of end stage renal disease worldwide with high morbidity and mortality. Glomerular mesangial cell (MC) proliferation, inflammatory cell infiltration and extracellular matrix (ECM) accumulation are the main pathological characteristics of DN. A previous study revealed that polycystin 1 N terminal fragment (PC 1 NF) fusion protein could inhibit ECM accumulation in a mesangial proliferative glomerulonephritis model. However, the role of PC 1 NF fusion protein in DN remains unknown. The results of the present study indicated that PC 1 NF fusion protein significantly abolished high glucose (HG) induced glomerular MC viability over three time points measured (24, 48 and 72 h) In addition, PC 1 NF suppressed the levels of monocyte chemotactic peptide 1 and tumor necrosis factor a, as well as the expression of fibronectin and collagen IV, in HG stimulated MCs. Furthermore, PC 1 NF fusion protein efficiently inhibited the activation of Wnt/b catenin signaling pathway in HG stimulated MCs. Taken together, these data indicated that PC 1 NF fusion protein inhibited HG induced MC proliferation, inflammation, and ECM expression via the modulation of the Wnt signaling pathway. The present study indicated that PC 1 NF fusion protein may be a potential agent in treating DN.
Experimental and therapeutic medicine