1. Interleukin-1β promotes the neurogenesis of carotid bodies by stimulating the activation of ERK1/2.
- Author
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Xue F, Liu L, Fan J, He S, Li R, Peng ZW, and Wang BR
- Subjects
- Animals, Blotting, Western, Glial Fibrillary Acidic Protein metabolism, Hypoxia physiopathology, Immunohistochemistry, Injections, Intraperitoneal, Interleukin-1beta administration & dosage, Male, Mice, Nestin metabolism, Phosphorylation, Photomicrography, Random Allocation, Rats, Sprague-Dawley, Recombinant Proteins administration & dosage, Recombinant Proteins metabolism, Tyrosine 3-Monooxygenase metabolism, Carotid Body physiology, Interleukin-1beta metabolism, MAP Kinase Signaling System physiology, Neurogenesis physiology
- Abstract
The carotid body (CB) is a complex sensory organ that functions to sense homeostatic O2 in the blood. Previous studies have shown that CBs express interleukin (IL)-1 receptor type I and that the chemosensitivity of CBs is increased following stimulation with pro-inflammatory cytokines. However, the effects of pro-inflammatory cytokines, such as IL-1β, on the neurogenesis of CB are unclear. Thus, in this study, we aimed to assess the effects of IL-1β and intermittent hypobaric hypoxia (IHH) plus IL-1β on the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, tyrosine hydroxylase (TH) and the expression of nestin, a well-established stem cell marker in the nervous system. The results showed that TH, nestin expression and ERK1/2 phosphorylation were increased in the rat CB following intraperitoneal injection of IL-1β. Moreover, IL-1β had additive effects on IHH. These results suggested that the plasticity of CB was increased following treatment with IL-1β and that ERK1/2 may be involved in neurogenic signaling in CBs., (Copyright © 2015 Elsevier B.V. All rights reserved.)
- Published
- 2015
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