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敲低 ETS 原癌基因 1（ETS1）可通过调节 NOD、LRR 和富含亮氨酸重复序列蛋白 3（NLRP3）转录来减轻急性肾损伤患者肾小管上皮细胞的细胞焦亡。

Knocking down ETS Proto-oncogene 1 (ETS1) alleviates the pyroptosis of renal tubular epithelial cells in patients with acute kidney injury by regulating the NLR family pyrin domain containing 3 (NLRP3) transcription.

机构信息

Department of Nephrology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.

Department of Nephrology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

出版信息

Bioengineered. 2022 May;13(5):12927-12940. doi: 10.1080/21655979.2022.2079242.

DOI:10.1080/21655979.2022.2079242
PMID:35611792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275905/
Abstract

Acute kidney injury (AKI) has a high mortality rate, but its pathogenesis remains unclear Lipopolysaccharide (LPS)-mediated renal tubular epithelial pyroptosis is involved in the pathogenesis of AKI. NLR family of pyrin domains containing 3 (NLRP3) plays an important role in pyroptosis. To further understand the transcriptional regulation mechanism of NLRP3, the peripheral blood of patients with AKI was analyzed in this study, showing that the levels of NLRP3 and cell pyroptosis in patients with AKI were significantly higher than those in normal controls. Furthermore, elevated levels of NLRP3 and cell pyroptosis were found in renal tubular epithelial cells after LPS treatment. Transcription factor ETS Proto-Oncogene 1 (ETS1) could bind to the upstream promoter transcription site of NLRP3 to transactivate NLRP3 in renal tubular epithelial cells. The cell pyroptosis level also decreased by knocking down ETS1. It is concluded that knocking down of ETS1 may reduce the renal tubular epithelial pyroptosis by regulating the transcription of NLRP3, thus relieving AKI. ETS1 is expected to be a molecular target for the treatment of AKI.

摘要

急性肾损伤 (AKI) 死亡率高，但发病机制尚不清楚。脂多糖 (LPS) 介导的肾小管上皮细胞焦亡参与 AKI 的发病机制。含 pyrin 结构域的 NOD 样受体家族 3 (NLRP3) 在焦亡中起重要作用。为了进一步了解 NLRP3 的转录调控机制，本研究分析了 AKI 患者的外周血，结果表明 AKI 患者的 NLRP3 水平和细胞焦亡明显高于正常对照组。此外，在 LPS 处理后，肾小管上皮细胞中也发现 NLRP3 和细胞焦亡水平升高。转录因子 ETS 原癌基因 1 (ETS1) 可与 NLRP3 的上游启动子转录位点结合，在肾小管上皮细胞中转录激活 NLRP3。敲低 ETS1 后，细胞焦亡水平也降低。结论：敲低 ETS1 可能通过调节 NLRP3 的转录减少肾小管上皮细胞焦亡，从而缓解 AKI。ETS1 有望成为 AKI 治疗的分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/d087d9317289/KBIE_A_2079242_F0005_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/b1b98b622113/KBIE_A_2079242_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/384d5d09eb0a/KBIE_A_2079242_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/d087d9317289/KBIE_A_2079242_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/43e10a4d067c/KBIE_A_2079242_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/93cc6354d9a9/KBIE_A_2079242_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/fb352361a18b/KBIE_A_2079242_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/b1b98b622113/KBIE_A_2079242_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/384d5d09eb0a/KBIE_A_2079242_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7c9/9275905/d087d9317289/KBIE_A_2079242_F0005_OC.jpg

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