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在结肠炎症模型中,OGR1 (GPR68) 和TDAG8 (GPR65) 具有对抗作用

Leonie Perren¹, Moana Busch¹, Cordelia Schuler¹

¹Department of Gastroenterology and Hepatology, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland.

International journal of molecular sciences

|October 14, 2023

概括

G蛋白结合受体卵巢癌GPR1 (OGR1) 和T细胞死亡相关基因8 (TDAG8) 在炎症性肠病中发挥作用. 缺少OGR1可以减轻肠道损伤,这表明这两种药物都是潜在的治疗点.

科学领域:

胃肠道学和免疫学
分子和细胞生物学分子和细胞生物学

背景情况:

像卵巢癌GPR1 (OGR1/GPR68) 和T细胞死亡相关基因8 (TDAG8/GPR65) 这样的G蛋白结合受体 (GPRs) 是与炎症性肠病 (IBD) 相关的pH传感器.
OGR1和TDAG8在炎症中表现出相反的作用,需要了解它们的主要生理相关性.

研究的目的:

研究OGR1和TDAG8在肠道炎症的小鼠模型中的单独和联合作用.
确定在IBD中调解炎症反应和肠道损伤的主要受体.

主要方法:

利用了自发性和急性小鼠结肠炎模型,对OGR1和TDAG8.8的向基因删除进行了向.
通过临床评分评估疾病严重程度,并使用定量聚合酶链反应 (qPCR) 和流细胞计 (FACS) 分析结肠组织.

主要成果:

在急性结肠炎中,OGR1缺陷显著降低了临床评分,而TDAG8缺陷或联合缺陷与野生型 (WT) 没有显著差异.
在自发性结肠炎中,OGR1缺乏减少了炎症,而TDAG8缺乏加剧了炎症. 与TDAG8缺乏的小鼠相比,三次淘汰的小鼠显示炎症减少.
缺少OGR1在TDAG8缺乏的小鼠中减少了促炎性细胞因子,并缓解了与TDAG8缺乏相关的肠损伤,这与IFNγ+T淋巴细胞和IL-23T辅助细胞的增加有关.

结论:

OGR1在肠道炎症中起着重要的保护作用,抵消TDAG8缺乏的有害影响.
OGR1和TDAG8都被确定为治疗炎症性肠病的潜在治疗点.

关键词:

克罗恩氏病是什么克罗恩氏病是什么在OGR1/GPR68中使用.在TDAG8/GPR65中使用.炎症性肠病是一种炎症性肠病.感应pH的G蛋白合受体是感应pH的.性结肠炎是一种

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