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在肥胖相关糖尿病的体内小鼠模型和体外大鼠模型中,凝血酶反应性脑周细胞对血脑屏障功能障碍的作用

Contribution of thrombin-reactive brain pericytes to blood-brain barrier dysfunction in an in vivo mouse model of obesity-associated diabetes and an in vitro rat model.

作者信息

Machida Takashi, Takata Fuyuko, Matsumoto Junichi, Miyamura Tomoyuki, Hirata Ryosuke, Kimura Ikuya, Kataoka Yasufumi, Dohgu Shinya, Yamauchi Atsushi

机构信息

Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.

BBB Laboratory, PharmaCo-Cell Co., Ltd., Nagasaki, Japan.

出版信息

PLoS One. 2017 May 10;12(5):e0177447. doi: 10.1371/journal.pone.0177447. eCollection 2017.

Abstract

Diabetic complications are characterized by the dysfunction of pericytes located around microvascular endothelial cells. The blood-brain barrier (BBB) exhibits hyperpermeability with progression of diabetes. Therefore, brain pericytes at the BBB may be involved in diabetic complications of the central nervous system (CNS). We hypothesized that brain pericytes respond to increased brain thrombin levels in diabetes, leading to BBB dysfunction and diabetic CNS complications. Mice were fed a high-fat diet (HFD) for 2 or 8 weeks to induce obesity. Transport of i.v.-administered sodium fluorescein and 125I-thrombin across the BBB were measured. We evaluated brain endothelial permeability and expression of tight junction proteins in the presence of thrombin-treated brain pericytes using a BBB model of co-cultured rat brain endothelial cells and pericytes. Mice fed a HFD for 8 weeks showed both increased weight gain and impaired glucose tolerance. In parallel, the brain influx rate of sodium fluorescein was significantly greater than that in mice fed a normal diet. HFD feeding inhibited the decline in brain thrombin levels occurring during 6 weeks of feeding. In the HFD fed mice, plasma thrombin levels were significantly increased, by up to 22%. 125I-thrombin was transported across the BBB in normal mice after i.v. injection, with uptake further enhanced by co-injection of unlabeled thrombin. Thrombin-treated brain pericytes increased brain endothelial permeability and caused decreased expression of zona occludens-1 (ZO-1) and occludin and morphological disorganization of ZO-1. Thrombin also increased mRNA expression of interleukin-1β and 6 and tumor necrosis factor-α in brain pericytes. Thrombin can be transported from circulating blood through the BBB, maintaining constant levels in the brain, where it can stimulate pericytes to induce BBB dysfunction. Thus, the brain pericyte-thrombin interaction may play a key role in causing BBB dysfunction in obesity-associated diabetes and represent a therapeutic target for its CNS complications.

摘要

糖尿病并发症的特征是位于微血管内皮细胞周围的周细胞功能障碍。随着糖尿病的进展,血脑屏障(BBB)表现出通透性增加。因此,血脑屏障处的脑周细胞可能参与中枢神经系统(CNS)的糖尿病并发症。我们假设脑周细胞对糖尿病时脑凝血酶水平升高做出反应,导致血脑屏障功能障碍和糖尿病中枢神经系统并发症。给小鼠喂食高脂饮食(HFD)2周或8周以诱导肥胖。测量静脉注射荧光素钠和125I-凝血酶通过血脑屏障的转运。我们使用共培养的大鼠脑内皮细胞和周细胞的血脑屏障模型,在凝血酶处理的脑周细胞存在的情况下评估脑内皮通透性和紧密连接蛋白的表达。喂食HFD 8周的小鼠体重增加且葡萄糖耐量受损。同时,荧光素钠的脑内流入率明显高于喂食正常饮食的小鼠。高脂饮食喂养抑制了喂食6周期间脑凝血酶水平的下降。在喂食高脂饮食的小鼠中,血浆凝血酶水平显著升高,高达22%。静脉注射后,125I-凝血酶在正常小鼠中可通过血脑屏障转运,未标记的凝血酶共同注射可进一步增强摄取。凝血酶处理的脑周细胞增加了脑内皮通透性,导致紧密连接蛋白-1(ZO-1)和闭合蛋白表达减少以及ZO-1形态紊乱。凝血酶还增加了脑周细胞中白细胞介素-1β、6和肿瘤坏死因子-α的mRNA表达。凝血酶可从循环血液通过血脑屏障转运,在脑中维持恒定水平,在那里它可刺激周细胞诱导血脑屏障功能障碍。因此,脑周细胞-凝血酶相互作用可能在肥胖相关糖尿病中导致血脑屏障功能障碍中起关键作用,并代表其中枢神经系统并发症的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b8/5425209/57a4f1378bfc/pone.0177447.g001.jpg

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