AngiotensinII AT-2 receptor nRNA is increased by hypoxic preconditioning(HP) in the brain and cerebellum of the neonatal rat

LOPEZ AGUILERA FRANCISCO; BIAGGIO VERONICA; SELTZER ALICIA

Huerta Grande Cordoba

Congreso; IIRCN II Reunion Conjunta de Neurociencias; 2010

Sociedad Argentina de Investigación en Neurociencias Taller Argentino de Neurociencias

Angiotensin II, an octapeptide compromised with mechanisms of organ injury and repair acts through the membrane receptors AT1-R and AT2-R. In previous experiments we observed a transient increase of AT2-R protein in the brain of preconditioned animals, on the following days after injury.  In this work we examined by RT-PCR the temporal expression of the AT2-R mRNA in the brain and cerebellum of WKY rat pups after being submitted to Hypoxia-Ischemia (HI-Les) on day8 after birth and treated with hypoxic-preconditioning 24h before injury (PCon). Control animals were sham operated and always breathed room air. On Day 1 after HI the PCon group showed a significant decrease of  the transcript (p<0.05)  in both brain hemispheres. On Day 2 after HI it was observed a remarkable increase of AT2-R mRNA in the lesioned side of the brains of Les and PCon animals (P<0.01), that returned to normal after a week. In the cerebellum  we observed significant increases on Day 2 (P<0.01) that persisted until day7 (p<0.05) only in the PCon group. (Statistical analysis: Anova one way, Bonferroni post test). The inflammatory response to the injury was assesed by IHC and confocal images of GFAP+ and Vim+ astrocytes in the Corpus Callosum were obtained and quantified. PCon animals showed less inflammation and no co-localization of AT2-R label with astrocyte markers. In conclusion: AT2-R is up-regulated in the brain in response to injury and hypoxic-preconditioning stimulates its cerebellar genomic expression. ANPCYT. PICT2006-451.