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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Minocycline alters expression of inflammatory markers in autonomic brain areas and ventilatory responses induced by acute hypoxia

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Author(s):
Silva, Talita M. [1] ; Chaar, Laiali J. [1] ; Silva, Reinaldo C. [2] ; Takakura, Ana C. [3] ; Camara, Niels O. [2] ; Antunes, Vagner R. [1] ; Moreira, Thiago S. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Dept Physiol & Biophys, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Dept Immunol, BR-05508000 Sao Paulo, SP - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 Sao Paulo, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Experimental Physiology; v. 103, n. 6, p. 884-895, JUN 1 2018.
Web of Science Citations: 5
Abstract

Prolonged and continuous exposure of mammals to a low oxygen environment (chronic hypoxia) elicits remarkable morphological and physiological adjustments. These include altered gene expression, increased peripheral chemosensitivity, enhanced respiratory drive and sympathoexcitation. The current study examines the hypothesis that acute hypoxia (AH) initiates an immune response in the central nervous system elicited by an increased expression of inflammatory mediators in specific brain areas related to autonomic control. Male Wistar rats pretreated with vehicle or minocycline (30mgkg(-1)day(-1) for 5 days) were subjected to AH (8% O-2, balance N-2) or normoxia (21% O-2) for 3h. AH increased interleukin (IL)-6, IL-1 and matrix metalloprotease 9 (MMP9) mRNA expression in the paraventricular nucleus of the hypothalamus (PVH) and rostral ventrolateral medulla (RVLM) and tumour necrosis factor (TNF) in the RVLM. Treatment with minocycline, an inhibitor of microglial activation, decreased IL-1, TNF and MMP9 mRNA expression in the RVLM, and increased IL-6 mRNA expression in the RVLM and PVH of rats exposed to AH. Minocycline treatment also elicited a decrease in the number of activated neurons in the RVLM/C1 neurons (expressed as Fos(+)/tyrosine hydroxylase(+)), the number of Fos-activated neurons in the PVH and the increase in ventilation elicited by AH. When viewed together, these results suggest that AH modulates the expression of inflammatory mediators in autonomic brain nuclei that may be involved in the responses to chemoreceptor activation. (AU)

FAPESP's process: 15/23376-1 - Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity
Grantee:Thiago dos Santos Moreira
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 16/23281-3 - Encephalic regions responsible for neuroplasticity observed in respiratory response induced by hypercapnia in a modelo of Parkinson's Disease
Grantee:Ana Carolina Takakura Moreira
Support Opportunities: Regular Research Grants
FAPESP's process: 16/22069-0 - Amelioration of the brainstem vascular imbalances in an spontaneously hypertensive rats with exercise
Grantee:Thiago dos Santos Moreira
Support Opportunities: Regular Research Grants
FAPESP's process: 16/21991-3 - Salt-induced hypertension: role of purinergic signaling in the neuronal cells at the hypothalamus level, and its correlation with the autonomic nervous system and blood pressure control
Grantee:Vagner Roberto Antunes
Support Opportunities: Regular Research Grants
FAPESP's process: 13/00401-5 - Integration between rostroventrolateral medulla and paraventricular nucleus during arterial chemoreceptor activation: possible involvement of catecholaminergic mechanisms
Grantee:Talita de Melo e Silva
Support Opportunities: Scholarships in Brazil - Doctorate