Immunohistochemical localization of galectins-1 and -3 and monitoring of tissue galectin-binding sites during tubular regeneration after renal ischemia reperfusion in the rat.

Endogenous lectins act as effectors of cellular activities such as growth regulation, migration and adhesion. In this study, we report the histochemical detection of galectins and their binding sites in rat kidneys after ischemic injury (35 min) with regard to renal regeneration. In this context, we have shown in a previous publication (Vansthertem et al., 2008) that extrarenal cells (CD44+, vimentin +) could be involved in this process of tubular restoration. In controls, galectin-1 is expressed by fusiform-shaped cells within cortical and medullar interstitium. Two days after ischemia, the number of positive interstitial cells increased temporarily within OSOM in the vicinity of altered tubules to later reach control level. After ischemia, we identified a population of galectin-3 (+), CD44 (+), and vimentin (+) interstitial round cells located in the outer stripe of outer medulla (OSOM) in the vicinity of necrotic tubules, but also in the lumen of adjacent blood vessels. The immunocytochemical characteristics of theses cells, along with their distribution within OSOM, suggest the involvement of a unique cell population during kidney regeneration. On the other hand, the distribution and density of binding sites for galectins within OSOM were not modified after ischemia and remained similar to controls. Altogether, our observations suggest that galectin-3 may be involved in the complex process of kidney regeneration following ischemia/reperfusion injury.