膜上皮细胞生长激素释放激素受体在膜上皮细胞炎症中的激素受体
Tengjiao Cui1,2, Medhi Wangpaichitr1, Andrew V Schally1,2,3
1Research Service, Miami VAHS, Miami, Florida, USA.
Experimental lung research
|August 16, 2023
概括
肺细胞中的生长激素释放激素受体 (GHRH-R) 驱动着炎症. 用MIA-602阻断GHR-R减少了促炎因素,这表明它在肺炎和纤维化中起作用.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 生长激素释放激素 (GHRH) 调节生长激素的分泌.
- 膜2型 (AT2) 细胞在肺炎和纤维化中起作用.
- 在AT2细胞中GHRH受体 (GHRH-R) 的存在和功能尚不清楚.
研究的目的:
- 研究GHRH-R在人类AT2细胞中的作用.
- 为了确定GHRH-R信号是否调节AT2细胞中的炎症和纤维性反应.
- 探索GHRH-R对抗剂在治疗肺炎中的潜力.
主要方法:
- 使用人类诱导的多能干细胞衍生AT2 (iAT2) 细胞.
- 用脂多糖 (LPS) 或亲纤维细胞因子刺激的iAT2细胞.
- 使用RT-PCR和西式涂抹,评估炎症和介质细胞标记物的基因和蛋白质表达.
- 研究了GHRH-R抗剂MIA-602对iAT2细胞反应的影响.
主要成果:
- 在iAT2细胞中,LPS和细胞因子诱导了促炎 (IL1-β,TNF-α) 和介酶体标记物.
- GHRH-R对手MIA-602显著抑制了LPS诱导的炎症性基因表达.
- 细胞因子暴露导致亲纤维基因 (TGFβ-1,Wnt5a) 和介酶蛋白 (N-cadherin,vimentin) 的表达增加.
结论:
- 人类iAT2细胞表达GHRH-R.
- 在AT2细胞中的GHRH-R信号传递有助于产生促炎因素.
- 准GHRH-R信号可能为肺炎和纤维化提供治疗策略.
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