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MicroRNA-142-5p facilitates the pathogenesis of ulcerative colitis by regulating SOCS1
Increasing evidence suggests that abnormal levels of microRNAs (miRNAs) are associated with ulcerative colitis (UC). It has been demonstrated that microRNA (miR)-142-5p was upregulated in UC patients. However, it remains unclear what the role of miR-142-5p is in UC. Samples from patients with active...
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Published in: | International journal of clinical and experimental pathology 2018-01, Vol.11 (12), p.5735-5744 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Increasing evidence suggests that abnormal levels of microRNAs (miRNAs) are associated with ulcerative colitis (UC). It has been demonstrated that microRNA (miR)-142-5p was upregulated in UC patients. However, it remains unclear what the role of miR-142-5p is in UC.
Samples from patients with active UC and healthy controls were performed with miRNA microarray to identify miRNAs involved in the pathogenesis of UC. The results of quantitative RT-PCR verified that miR-142-5p was upregulated in UC patients. Meanwhile, the decreased expression of suppressor of cytokine signaling 1 (SOCS1) was also detected at mRNA and protein levels. The regulatory effect of miR-142-5p on SOCS1 was evaluated by luciferase reporter assay. Levels of IL-6 or IL-8 were detected by quantitative RT-PCR or enzyme-linked immunosorbent assay in HT-29 cells to evaluate the roles of SOCS1 or miR-142-5p in the progression of UC.
The expression level of miR-142-5p was significantly upregulated and inversely correlated with SOCS1. Luciferase experiments showed that miR-142-5p interfered with the expression of SOCS1 by directly targeting its 3'-UTR. Furthermore, the level of miR-142-5p plays an important role in the secretion of IL-6 and IL-8. Moreover, lost function of SOCS1 reversed the miR-142-5p inhibitory effect.
These results indicate that miR-142-5p improved the intestinal inflammation of active-UC patients by downregulating SOCS1 expression and increasing the cytokines IL-6 and IL-8 secretion. |
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ISSN: | 1936-2625 |