Mineralocorticoid receptor associates with pro‐inflammatory bias in the hippocampus of spontaneously hypertensive rats

Journal of Neuroendocrinology - Tập 29 Số 7 - 2017
María Elvira Brocca1, Luciana Pietranera2,1, María Meyer1, Analı́a Lima1, P. Roig1, E. R. de Kloet3, Alejandro F. De Nicola2,1
1Laboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Buenos Aires, Argentina
2Department of Human Biochemistry, Faculty of Medicine, University of Buenos Aires, Buenos Aires, Argentina
3Division of Endocrinology, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands

Tóm tắt

Damage observed in the hippocampus of the adult spontaneously hypertensive rat (SHR) resembles the neuropathology of mineralocorticoid‐induced hypertension, supporting a similar endocrine dysfunction in both entities. In the present study, we 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. Accordingly, in the hippocampus, we measured mRNA expression and immunoreactivity of the MR and glucocorticoid receptor (GR) using a quantitative polymerase chain reaction and histochemistry. We also measured serum‐glucocorticoid‐activated kinase 1 (Sgk1 mRNA), the number and phenotype of Iba1+ microglia, as well as mRNA expression levels of the pro‐inflammatory factors cyclo‐oxygenase 2 (Cox2), Nlrp3 inflammasome and tumour necrosis factor α (Tnfα). Expression of anti‐inflammatory transforming growth factor (Tgf)β mRNA and the NADPH‐diaphorase activity of nitric oxide synthase (NOS) were also determined. The results showed that, in the hippocampus of SHR rats, expression of MR and the number of immunoreactive MR/GR co‐expressing cells were increased compared to Wistar‐Kyoto control animals. Expression of Sgk1, Cox2, Nlrp3 and the number of ramified glia cells positive for Iba1+ were also increased, whereas Tgfβ mRNA expression and the NADPH‐diaphorase activity of NOS were decreased. We propose that, in the SHR hippocampus, increased MR expression causes a bias towards a pro‐inflammatory phenotype characteristic for hypertensive encephalopathy.

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Journal of Neuroendocrinology

Tập 29 Số 7

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