Yu Zhang1,2,3, Xiaxin Wu1, Jinfeng Wu1, Shuang Li1, Sen Han4, Zhijie Lin4, Shizhen Ding4, Xiaoqin Jia4, Weijuan Gong1,2,4. 1. School of Nursing, Yangzhou University Yangzhou, China. 2. Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases Yangzhou, China. 3. Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Jiangsu Key Laboratory of Zoonosis, Yangzhou University Yangzhou, China. 4. Department of Immunology, School of Medicine, Yangzhou University Yangzhou, China.
Abstract
OBJECTIVE: Post-infectious irritable bowel syndrome (PI-IBS) is a common functional gastrointestinal (GI) disorder that occurs after acute GI infection. Recent studies showed that microRNAs were involved in the occurrence and development of IBS. Here, we elaborated the role of miR-510 in the occurrence of PI-IBS and analyzed its mechanism. METHODS: We detected the expressions of miR-510 and PRDX1 in colonic mucosal tissues by qRT-PCR, Western blot and immunohistochemistry. Furthermore, we transfected Caco-2 cells with miR-510 mimic, anti-miR-510, si-PRDX1, and control, then evaluated the cell viability and apoptosis by CCK8 assay and flow cytometry, assessed expression levels of PRDX1 by qRT-PCR and Western blot analysis, and pro-inflammatory cytokines by qRT-PCR and ELISA. RESULTS: MiR-510 expression was downregulated and negatively correlated with TNF-α, whereas PRDX1 expression was upregulated in PI-IBS colonic mucosal tissues. LPS at concentrations of 5 and 10 μg/ml can significantly induce inflammatory injury in Caco-2 cells. MiR-510 overexpression aggravated the injury induced by LPS, as reflected by increased cell viability, decreased apoptosis, and less production of pro-inflammatory cytokines. miR-510 mimic transfection in cells significantly suppressed the mRNA and protein expression levels of PRDX1. Furthermore, the inflammatory injury induced by LPS was exacerbated by upregulating PRDX1 expression when miR-510 was knocked down. CONCLUSION: MiR-510 downregulation in intestinal tissue might contribute to PI-IBS via targeting PRDX1. The results of this study will not only enrich the pathogenesis of PI-IBS but also make us understand the biological activity of miR-510 and provide important experimental basis for PI-IBS clinical treatment targeting miR-510. AJTR
OBJECTIVE: Post-infectious irritable bowel syndrome (PI-IBS) is a common functional gastrointestinal (GI) disorder that occurs after acute GI infection. Recent studies showed that microRNAs were involved in the occurrence and development of IBS. Here, we elaborated the role of miR-510 in the occurrence of PI-IBS and analyzed its mechanism. METHODS: We detected the expressions of miR-510 and PRDX1 in colonic mucosal tissues by qRT-PCR, Western blot and immunohistochemistry. Furthermore, we transfected Caco-2 cells with miR-510 mimic, anti-miR-510, si-PRDX1, and control, then evaluated the cell viability and apoptosis by CCK8 assay and flow cytometry, assessed expression levels of PRDX1 by qRT-PCR and Western blot analysis, and pro-inflammatory cytokines by qRT-PCR and ELISA. RESULTS:MiR-510 expression was downregulated and negatively correlated with TNF-α, whereas PRDX1 expression was upregulated in PI-IBS colonic mucosal tissues. LPS at concentrations of 5 and 10 μg/ml can significantly induce inflammatory injury in Caco-2 cells. MiR-510 overexpression aggravated the injury induced by LPS, as reflected by increased cell viability, decreased apoptosis, and less production of pro-inflammatory cytokines. miR-510 mimic transfection in cells significantly suppressed the mRNA and protein expression levels of PRDX1. Furthermore, the inflammatory injury induced by LPS was exacerbated by upregulating PRDX1 expression when miR-510 was knocked down. CONCLUSION:MiR-510 downregulation in intestinal tissue might contribute to PI-IBS via targeting PRDX1. The results of this study will not only enrich the pathogenesis of PI-IBS but also make us understand the biological activity of miR-510 and provide important experimental basis for PI-IBS clinical treatment targeting miR-510. AJTR
Authors: L W Dong; X N Sun; Z C Ma; J Fu; F J Liu; B L Huang; D C Liang; D M Sun; Cheng Lan Journal: BMC Gastroenterol Date: 2021-06-30 Impact factor: 3.067
Authors: Luis Alberto Bravo-Vázquez; Ixchel Medina-Ríos; Luis David Márquez-Gallardo; Josué Reyes-Muñoz; Francisco I Serrano-Cano; Surajit Pathak; Antara Banerjee; Anindya Bandyopadhyay; Asim K Duttaroy; Sujay Paul Journal: Dig Dis Sci Date: 2022-05-04 Impact factor: 3.487