Thyroid stimulating hormone aggravates diabetic retinopathy through the mitochondrial apoptotic pathway,Journal of Cellular Physiology

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Thyroid stimulating hormone aggravates diabetic retinopathy through the mitochondrial apoptotic pathway
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2021-08-25 , DOI: 10.1002/jcp.30563
Dong Lin _{1,

2,

3} , Ruijie Qin _{1,

2} , Lixin Guo _{1,

2}

Affiliation

Diabetic retinopathy (DR) is a common complication of diabetes mellitus. High glucose-induced mitochondrial apoptosis is involved in the loss of retinal pericytes (PCs), which is considered to be a predominant pathologic change of diabetic retinopathy (DR). A high thyroid stimulating hormone (TSH) serum level is associated with an increased prevalence of DR in diabetic patients. Here, we investigated whether TSH regulated glucose-induced PCs loss through TSH-receptor (TSHR)-dependent mitochondrial apoptosis. First, the serum TSH level was found to be an independent risk factor for DR in Type 2 diabetic study participants (odds ratio = 2.294; 95% confidence interval: 1.925–2.733; p ≤ 0.001). Second, human PCs were treated with different concentrations of glucose, with or without bovine TSH (b-TSH). Glucose induced mitochondrial apoptosis through various mechanisms, including through regulating the expression of apoptosis-related proteins and inducing mitochondrial dysfunction, which could be deteriorated by costimulation of glucose and b-TSH. Additionally, we detected functional TSHR in PCs; blocking TSHR significantly restricted TSH-induced apoptosis. Thus, the presence of functional TSHR in human retinal PCs may facilitate the effect of high TSH on high glucose-induced PCs loss through TSHR-dependent mitochondrial apoptosis.

中文翻译：

促甲状腺激素通过线粒体凋亡途径加重糖尿病视网膜病变

糖尿病视网膜病变（DR）是糖尿病的常见并发症。高糖诱导的线粒体凋亡与视网膜周细胞 (PC) 的丢失有关，这被认为是糖尿病视网膜病变 (DR) 的主要病理变化。高促甲状腺激素 (TSH) 血清水平与糖尿病患者 DR 患病率增加有关。在这里，我们研究了 TSH 是否通过 TSH 受体 (TSHR) 依赖性线粒体凋亡调节葡萄糖诱导的 PC 损失。首先，血清 TSH 水平被发现是 2 型糖尿病研究参与者 DR 的独立危险因素（优势比 = 2.294；95% 置信区间：1.925–2.733；p ≤ 0.001)。其次，人类 PC 用不同浓度的葡萄糖处理，有或没有牛 TSH (b-TSH)。葡萄糖通过多种机制诱导线粒体凋亡，包括通过调节凋亡相关蛋白的表达和诱导线粒体功能障碍，葡萄糖和b-TSH的共刺激可能使线粒体功能障碍恶化。此外，我们在 PC 中检测到功能性 TSHR；阻断 TSHR 显着限制了 TSH 诱导的细胞凋亡。因此，人视网膜 PC 中功能性 TSHR 的存在可能促进高 TSH 通过 TSHR 依赖性线粒体凋亡对高葡萄糖诱导的 PC 损失的影响。

更新日期：2021-08-25

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