Mineralocorticoid receptor and inflammation in the hippocampus of spontaneously hypertensive rats

A.F. DE NICOLA; L. PIETRANERA; M.E. BROCCA; A. LIMA; N. PILONI; P. ROIG; M. MEYER

Madrid

Jornada; Jornadas Junior 2017; 2017

Instituto Cajal

Damage observed in the hippocampus of the adult spontaneously hypertensive rat (SHR) resembles the neuropathology of mineralocorticoid-induced hypertension, consistent with a similar endocrine dysfunction in both. In this study we have tested the hypothesis that increased expression of the hippocampal mineralocorticoid receptor (MR) in SHR animals is associated with a prevalent expression of pro-inflammatory over anti-inflammatory factors. For this purpose, we measured hippocampal mRNA expression and immunoreactivity of the MR and the glucocorticoid receptor (GR) using qPCR and histochemistry. We also measured the serum-glucocorticoid-activated kinase 1 (Sgk1) mRNA, the number and phenotype of Iba1+ microglia, mRNA expression levels of the proinflammatory factors cyclooxygenase 2 (Cox2), Nlrp3 inflammasome and tumor necrosis factor alpha (TNFa). Expression of anti-inflammatory Tgfb mRNA and the activity of nitric oxide synthase (NOS) were also determined. In the hippocampus of SHR rats expression of MR and number of immunoreactive MR / GR co-expressing cells is increased over Wistar Kyoto control animals. Expression of Sgk1, Cox2, Nlrp3 and the number of ramified glia cells positive for Iba1+ also increased, while Tgfb mRNA expression and NOS decreased. We propose that in SHR hippocampus increased MR expression causes a bias towards a pro-inflammatory phenotype characteristic of hypertensive encephalopathy.