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通过结合TAF1减少LncR-GAS5的腺因基转移酶表达,以增加CIH造成的脏损伤

Wei Liu^1,2, Wukaiyang Liang^1,2, CunTai Zhang^1,2

¹Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, China.

|July 12, 2024

概括

长非编码RNA GAS5与TAF1结合,抑制APRT,使老鼠的慢性间歇性缺氧诱导的损伤恶化. 减少GAS5或增加APRT可以缓解损伤,亡和纤维化.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

阻塞性睡眠呼吸暂停-呼吸暂停综合征 (OSAHS) 通过慢性间歇性缺氧 (CIH) 诱导的损伤引起慢性病 (CKD).
在CIH诱导的损伤中,长非编码RNA (lncRNA) GAS5和腺因基转移酶 (APRT) 之间的相互作用尚不清楚.

研究的目的:

在CIH诱导的损伤的背景下,研究lncRNA GAS5和APRT之间的相互作用.
阐明CIH诱导的损伤背后的分子机制,涉及GAS5和APRT.

主要方法:

建立了慢性间歇性缺氧 (CIH) 的大鼠模型.
使用了转录组测序,等离子体转染 (sh-GAS5,OE-APRT),RT-qPCR,西部涂抹和TUNEL染色.
执行RNA拉下,RIP和ChIP测试以验证分子相互作用.

主要成果:

在大鼠脏中,CIH显著增加TAF1并降低APRT表达.
GAS5抑制或APRT过度表达减轻了CIH诱导的损伤,降低了BUN和肌素水平.
发现GAS5和TAF1对APRT转录有负面调节,其中GAS5与TAF1.1结合.

结论:

lncRNA GAS5与TAF1相互作用以抑制APRT转录.
这种相互作用加剧了老鼠的慢性间歇性缺氧诱导的损伤.
针对GAS5-TAF1-APRT轴可能为CIH相关脏疾病提供治疗潜力.

关键词:

APRT APRT APRT 的意思是什么意思一个CIH的CIH是一个CIH.造成脏损伤的人.在TAF1中,TAF1是TAF1.在cRNA GAS5 中.

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