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抗 miR-141-3p 通过靶向大鼠胎儿腰骶部排便中枢中的 Yy1 维持自噬与凋亡之间的稳态。

Anti-miR-141-3p maintains homeostasis between autophagy and apoptosis by targeting Yy1 in the fetal lumbosacral defecation center of rats.

作者信息

Li Yue, Liu Peiqi, Yao Yifan, Wang Weilin, Jia Huimin, Bai Yuzuo, Yuan Zhengwei, Yang Zhonghua

机构信息

Department of Pediatric Surgery, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning, China.

Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning, China.

出版信息

Mol Ther Nucleic Acids. 2024 Mar 6;35(2):102163. doi: 10.1016/j.omtn.2024.102163. eCollection 2024 Jun 11.

Abstract

Anorectal malformations (ARMs) are congenital diseases that lead to postoperative fecal incontinence, constipation, and soiling, despite improvements in surgery; however, their pathological mechanisms remain unclear. Here, we report the role of microRNA-141-3p in maintaining homeostasis between apoptosis and autophagy in the lumbosacral defecation center of fetal rats with ARMs. Elevated microRNA-141-3p expression inhibited YIN-YANG-1 expression by binding its 3' UTR, and repressed autophagy and triggered apoptosis simultaneously. Then, adenylate cyclase 3 was screened to be the downstream target gene of YIN-YANG-1 by chromatin immunoprecipitation sequencing experiments, and Yin Yang 1 could positively activate the transcription of adenylate cyclase 3 by directly interacting with the motif GAGATGG and ATGG in its promoter. Intraamniotic microinjection of adeno-rno-microRNA-141-3p-sponge-GFP in fetal rats with ARMs on embryonic day 15 restored apoptosis-autophagy homeostasis. These findings reveal that microRNA-141-3p upregulation impaired homeostasis between apoptosis and autophagy by inhibiting the YIN-YANG-1/adenylate cyclase 3 axis, and that intraamniotic injection of anti-microRNA-141-3p helped maintain homeostasis in the lumbosacral defecation center of ARMs during embryogenesis.

摘要

肛门直肠畸形(ARMs)是一种先天性疾病,尽管手术有所改进,但仍会导致术后大便失禁、便秘和便污;然而,其病理机制仍不清楚。在此,我们报告了微小RNA-141-3p在维持患有ARMs的胎鼠腰骶部排便中枢细胞凋亡和自噬之间的稳态中的作用。微小RNA-141-3p表达升高通过结合其3'UTR抑制阴阳-1表达,同时抑制自噬并引发细胞凋亡。然后,通过染色质免疫沉淀测序实验筛选出腺苷酸环化酶3是阴阳-1的下游靶基因,阴阳-1可通过直接与腺苷酸环化酶3启动子中的基序GAGATGG和ATGG相互作用来正向激活其转录。在胚胎第15天对患有ARMs的胎鼠进行羊膜腔内微量注射腺病毒-微小RNA-141-3p海绵-GFP可恢复细胞凋亡-自噬稳态。这些发现揭示,微小RNA-141-3p上调通过抑制阴阳-1/腺苷酸环化酶3轴损害细胞凋亡和自噬之间的稳态,并且羊膜腔内注射抗微小RNA-141-3p有助于在胚胎发育过程中维持ARMs腰骶部排便中枢的稳态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f80/10965809/b448c2b4364c/fx1.jpg

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