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miR-199a-3p 通过靶向 MTOR 调节 HCT-8 细胞自噬和凋亡对微小隐孢子虫感染的反应。

MiR-199a-3p regulates HCT-8 cell autophagy and apoptosis in response to Cryptosporidium parvum infection by targeting MTOR.

机构信息

College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.

Key Laboratory of Quality and Safety Control of Poultry Products, Ministry of Agriculture and Rural Affairs, Zhengzhou, 450046, China.

出版信息

Commun Biol. 2024 Jul 31;7(1):924. doi: 10.1038/s42003-024-06632-5.

DOI:10.1038/s42003-024-06632-5
PMID:39085368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11291649/
Abstract

The microRNAs (miRNAs) of their hosts play an important role in regulating both the innate and adaptive immune responses to Cryptosporidium parvum infection. The mechanisms of autophagy and apoptosis are important components of the defense system against C. parvum infection. In this study, we investigate the role of miRNA-199a-3p in regulating MTOR-mediated autophagy and apoptosis in HCT-8 cells induced by C. parvum. The expression of miR-199a-3p increased at 3, 6 and 12 hours postinfection (hpi) but decreased at 24 and 48 hpi. The upregulation of miR-199a-3p promoted autophagy and apoptosis and limited the parasite burden in HCT-8 cells after C. parvum infection. The downregulation of miR-199a-3p inhibited the autophagy and apoptosis induced by C. parvum and enhanced the parasite burden in HCT-8 cells. A luciferase reporter showed that MTOR was a target gene of miR-199a-3p. Suppressed expression of MTOR by small interfering RNA (siRNA) promoted autophagy and apoptosis and limited C. parvum burden in HCT-8 cells. Co-transfection with miR-199a-3p inhibitor or si-mTOR revealed that miR-199a-3p regulates autophagy and apoptosis in HCT-8 cells through MTOR, to resist C. parvum infection. In conclusion, intestinal epithelial cells defend against C. parvum infection by regulating their autophagy and apoptosis through the miR-199a-3p-MTOR axis.

摘要

宿主的 microRNAs (miRNAs) 在调节对微小隐孢子虫感染的先天和适应性免疫反应方面发挥着重要作用。自噬和细胞凋亡的机制是抵御微小隐孢子虫感染的防御系统的重要组成部分。在这项研究中，我们研究了 miRNA-199a-3p 在调节 MTOR 介导的自噬和凋亡中的作用，这些自噬和凋亡是由微小隐孢子虫感染 HCT-8 细胞引起的。miR-199a-3p 的表达在感染后 3、6 和 12 小时（hpi）增加，但在 24 和 48 hpi 时减少。miR-199a-3p 的上调促进了自噬和凋亡，并限制了微小隐孢子虫感染后 HCT-8 细胞中的寄生虫负担。miR-199a-3p 的下调抑制了微小隐孢子虫诱导的自噬和凋亡，并增强了 HCT-8 细胞中的寄生虫负担。荧光素酶报告显示 MTOR 是 miR-199a-3p 的靶基因。通过小干扰 RNA (siRNA) 抑制 MTOR 的表达促进了自噬和凋亡，并限制了 HCT-8 细胞中的微小隐孢子虫负担。共转染 miR-199a-3p 抑制剂或 si-MTOR 表明，miR-199a-3p 通过 MTOR 调节 HCT-8 细胞中的自噬和凋亡，以抵抗微小隐孢子虫感染。总之，肠上皮细胞通过 miR-199a-3p-MTOR 轴调节自噬和凋亡来抵抗微小隐孢子虫感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/e818047770ee/42003_2024_6632_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/85e1f409d11f/42003_2024_6632_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/1d76e3adc9fd/42003_2024_6632_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/21c5543e5ff8/42003_2024_6632_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/d4dc493b95f4/42003_2024_6632_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/e818047770ee/42003_2024_6632_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/85e1f409d11f/42003_2024_6632_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/1d76e3adc9fd/42003_2024_6632_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/21c5543e5ff8/42003_2024_6632_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/d4dc493b95f4/42003_2024_6632_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89aa/11291649/e818047770ee/42003_2024_6632_Fig5_HTML.jpg

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