MicroRNA-24 inhibits serotonin reuptake transporter expression and aggravates irritable bowel syndrome
| Autor: | Qin Wang, Guangen Yang, Weiming Mao, Xiujun Liao, Shuxian Shao, Wenjing Wu |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Biophysics Down-Regulation Biology Biochemistry Irritable Bowel Syndrome Pathogenesis Mice 03 medical and health sciences Downregulation and upregulation Intestinal mucosa Western blot Internal medicine microRNA medicine Animals Humans Intestinal Mucosa Molecular Biology Cells Cultured Irritable bowel syndrome Serotonin Plasma Membrane Transport Proteins Regulation of gene expression Mice Inbred BALB C medicine.diagnostic_test Cell Biology medicine.disease MicroRNAs 030104 developmental biology Endocrinology Gene Expression Regulation |
| Zdroj: | Biochemical and Biophysical Research Communications. 469:288-293 |
| ISSN: | 0006-291X |
| Popis: | Irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal disorder. MicroRNAs (miRNAs) have been widely demonstrated to take part in various physiological and pathological processes. In the present study, the role of miR-24 in the pathogenesis of IBS and the potential mechanism in this process were evaluated. Human intestinal mucosa epithelial cells of colon from IBS patients and healthy subjects were collected. An IBS mouse model was established with the induction of trinitro-benzene-sulfonic acid (TNBS). The expression levels of miR-24 and serotonin reuptake transporter (SERT) were analyzed using Real-time PCR and western blot in both human specimen and mice. miR-24 was upregulated in IBS patients and mice intestinal mucosa epithelial cells. Luciferase reporter assay showed that SERT was a potential target gene of miR-24. The treatment of miR-24 inhibitor increased pain threshold and nociceptive threshold levels and reduced MPO activity in proximal colon of IBS mice, and up-regulated the mRNA and protein expression levels of SERT in intestinal mucosa epithelial cells. miR-24 played a role in the pathogenesis of IBS probably through regulating SERT expression. |
| Databáze: | OpenAIRE |
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