Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice

CD146 is an endothelial junctional adhesion molecule, which expression increased in human glomerular diseases. However, the pathological significance of this overexpression remains unknown. Induction glomerulonephritis mice, by using nephrotoxic serum, showed that was highly induced within damaged glomeruli and associated with renal inflammation fibrosis. Interestingly, 2 weeks after induction, knockout mice preserved function as proteinuria blood urea nitrogen levels were significantly lower compared wild-type littermates. Furthermore, structure considerably conserved, since crescents formation, tubular dilation, monocyte lymphocyte infiltration, interstitial fibrosis reduced. Colocalization markers for different types cells mainly injured endothelium tuft. Consequently, we generated a new transgenic strain specifically deleted vascular endothelium. Similarly to knockout, these preservation induction animals. These data show plays major role may represent novel therapeutic target reduce damage progression disease.