Age-related changes in regulator of G-protein signaling (RGS)-10 expression in peripheral and central immune cells may influence the risk for age-related degeneration

被引:20
作者
Kannarkat, George T. [1 ]
Lee, Jae-Kyung [1 ]
Ramsey, Chenere P. [1 ]
Chung, Jaegwon [1 ]
Chang, Jianjun [1 ]
Porter, Isadora [1 ]
Oliver, Danielle [1 ]
Shepherd, Kennie [2 ]
Tansey, Malu G. [1 ]
机构
[1] Emory Univ, Sch Med, Dept Physiol, Atlanta, GA 30322 USA
[2] Morehouse Sch Med, Dept Pharmacol & Toxicol, Atlanta, GA 30310 USA
基金
美国国家卫生研究院;
关键词
Aging; Dopamine; Immune cells; Midbrain; Oxidative stress; RGS10; Tyrosine hydroxylase; GTPASE-ACTIVATING PROTEINS; ASSOCIATION; COMPLEX; GENES; MOUSE; RGS;
D O I
10.1016/j.neurobiolaging.2015.02.006
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Inflammation in the aging brain increases risk for neurodegenerative disease. In humans, the regulator of G-protein signaling-10 (RGS10) locus has been associated with age-related maculopathy. Chronic peripheral administration of lipopolysaccharide in the RGS10-null mice induces nigral dopaminergic (DA) degeneration, suggesting that RGS10 modulates neuroimmune interactions and may influence susceptibility to neurodegeneration. Because age is the strongest risk factor for neurodegenerative disease, we assessed whether RGS10 expression changes with age and whether aged RGS10-null mice have altered immune cell profiles. Loss of RGS10 in aged mice does not alter the regulation of nigral DA neurons but does alter B-cell, monocyte, microglial, and CD4+ T-cell populations and inflammatory cytokine levels in the cerebrospinal fluid. These results suggest that loss of RGS10 is associated with an age-dependent dysregulation of peripheral and central immune cells rather than dysregulation of DA neuron function. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:1982 / 1993
页数:12
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