Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury
Figure 7
Distribution of NCAM-positive cells (left column) and of -SMA-positive cells (right column) in the renal interstitium of control (a, b, e, f) or at different time intervals after ischemia-reperfusion (c, d, g, h). In control, NCAM-positive interstitial cells formed a loose network around cortical tubules (a) but with a higher density in ISOM (e). The density of positive cells in OSOM increased 16 hours after reperfusion mainly in the vicinity of altered tubules (c). Sometimes isolated epithelial cells appeared positive in altered tubules of OSOM (c inset). Within ISOM, the density of positive cells increased 12 hours after ischemia and remains high during the two following weeks (g). In control kidneys, the immunolabeling with an anti--SMA antibody was limited to the media of arteriolar vessels (b) and to pericytes of the ascending vasa recta in the vascular bundles of ISOM (f). Two weeks after reperfusion, -SMA immunoreactivity is present in flattened cells surrounding precystic tubules (d) while ISOM remained similar to controls (h). Scale bar. : (a–h).
