Interleukin-1β promotes the neurogenesis of carotid bodies by stimulating the activation of ERK1/2

Interleukin-1β promotes the neurogenesis of carotid bodies by stimulating the activation of ERK1/2
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Interleukin-1β 通过刺激 ERK1/2 的激活促进颈动脉体的神经发生

DOI:
10.1016/j.resp.2015.08.008
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发表时间:
2015-12-01
影响因子:
2.3
通讯作者:
Wang, Bai-Ren
Wang, Bai-Ren
中科院分区:
医学4区
文献类型:
--
作者:
Xue, Fen;Liu, Ling;Wang, Bai-Ren

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The carotid body (CB) is a complex sensory organ that functions to sense homeostatic O-2 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-1 beta, on the neurogenesis of CB are unclear. Thus, in this study, we aimed to assess the effects of IL-1 beta and intermittent hypobaric hypoxia (IHH) plus IL-1 beta 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-1 beta. Moreover, IL-1 beta had additive effects on IHH. These results suggested that the plasticity of CB was increased following treatment with IL-1 beta and that ERK1/2 may be involved in neurogenic signaling in CBs. (C) 2015 Elsevier B.V. All rights reserved.