Monoclonal antibody to CD31 (PECAM-1) inhibits tubular regeneration after ischemia reperfusion injury in the rat.

Aims: We used a rat model of renal ischemia (35 min) to test the potential involvement of platelet/endothelial cell adhesion molecule 1 (PECAM-1/CD31) in the process of S3 tubule regeneration.

Methods: A monoclonal antibody specific for murine PECAM-1 was injected i.p.

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.

Expression of nestin, vimentin, and NCAM by renal interstitial cells after ischemic tubular injury.

This work explores the distribution of various markers expressed by interstitial cells in rat kidneys after ischemic injury (35 minutes) during regeneration of S3 tubules of outer stripe of outer medulla (OSOM). Groups of experimental animals (n = 4) were sacrificed every two hours during the first 24 hours post-ischemia as well as 2, 3, 7, 14 days post-ischemia. The occurrence of lineage markers was analyzed on kidney sections by immunohistochemistry and morphometry during the process of tubular regeneration.

Label-retaining cells and tubular regeneration in postischaemic kidney.

Background: In this study, we have examined rat kidneys after ischaemic injury (35 min) with regard to the dynamics of S3 tubule regeneration.

Methods: One day before ischaemia, each rat received four successive i.p.