Differential mRNA expression of neuroinflammatory modulators in the spinal cord and thalamus of type 2 diabetic monkeys.
Differential mRNA expression of neuroinflammatory modulators in the spinal cord and thalamus of type 2 diabetic monkeys.
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DOI：
10.1111/1753-0407.12780
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发表时间：
2018-11
影响因子：
4.5
通讯作者：
Ko MC
中科院分区：
文献类型：
--
作者：
Ding H;Kiguchi N;Kishioka S;Ma T;Peters CM;Ko MC
鉴于糖尿病相关并发症与神经炎症密切相关，研究糖尿病灵长类动物中枢神经系统炎症调节剂的潜在变化势在必行。采用逆转录和实时定量聚合酶链式反应技术，比较了自然发生的2型糖尿病猴和正常对照组大鼠脊髓背角(SDH)和丘脑中促炎症和抗炎细胞因子、Toll样受体(TLR)、生长因子和大麻素受体的表达水平。在糖尿病猴的琥珀酸脱氢酶中，我们观察到促炎症细胞因子(即白介素1β和肿瘤坏死因子α)、白介素1和肿瘤坏死因子α的基因水平升高，而抗炎细胞因子白介素10的基因水平降低。生长因子和大麻素受体的mRNA水平无明显变化。与基因数据一致的是，糖尿病猴的肿瘤坏死因子α免疫反应也显著增强。此外，白介素1β、肿瘤坏死因子α、TLR1mRNA和TLR2mRNA的表达水平与血糖水平呈正相关。参与神经炎症的几种配体和受体在糖尿病猴子的脊髓中同时处于失调状态。这一灵长类疾病模型将有助于设计新的治疗方法来改善糖尿病患者的神经炎症驱动的不良反应。
Given that diabetes-associated complications are closely associated with neuroinflammation, it is imperative to study potential changes in neuroinflammatory modulators in the central nervous system of diabetic primates. The mRNA levels of pro-inflammatory and anti-inflammatory cytokines, toll-like receptors (TLR), growth factors, and cannabinoid receptors were compared in the spinal dorsal horn (SDH) and thalamus of naturally occurring type 2 diabetic monkeys and an age-matched control group using reverse transcription and quantitative real-time polymerase chain reaction. In the SDH of diabetic monkeys, we observed increases in the mRNA levels of pro-inflammatory cytokines (i.e., interleukin-1β and tumor necrosis factor-α (TNFα)), TLR1, and TLR2, and decreases in the mRNA levels of interleukin-10, an anti-inflammatory cytokine. No changes were observed in the mRNA levels of growth factors and cannabinoid receptors. In line with the mRNA data, TNFα-immunoreactivity was also significantly increased in diabetic monkeys. Moreover, the mRNA expression levels of interleukin-1β, TNFα, TLR1, and TLR2 in the SDH were positively correlated with plasma glucose levels in all monkeys. Several ligands and receptors involved in neuroinflammation are simultaneously dysregulated in the spinal cord of diabetic monkeys. This primate disease model will facilitate the design of novel treatment approaches to ameliorate neuroinflammation-driven adverse effects in diabetic patients.
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影响因子：
120.1
作者：
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