Lou Chunyan, Li Yanyang
Department of Pediatrics, Huaihe Hospital of Henan University, No. 8, Baobei Road, Gulou District, Kaifeng, 475000 China.
J Inflamm (Lond). 2018 Apr 6;15:7. doi: 10.1186/s12950-018-0181-z. eCollection 2018.
Inflammatory bowel disease (IBD) is one of the chronic gastrointestinal diseases with increasing risk of colon cancer development in the future. Apoptosis and inflammation play an important role in the etiology of this disease. MicroRNAs are associated with etiology of different diseases including IBD. In this study, we aimed to explore the role of miR-135a in the etiology of colitis in murine model of DSS-induced colitis.
The results showed that expression of miR-135a in colonic cells was suppressed and up-regulating miR-135a inhibited apoptosis and inflammation of colonic epithelial cells. Additionally, Hif1α was identified as the target gene of miR-135a which promoted apoptosis and inflammation as knockdown of Hif1α led to the suppression of both apoptosis and inflammation.
Overexpression of miR-135a might be beneficial in IBD due to its anti-apoptosis and anti-inflammation effects in vitro.
炎症性肠病(IBD)是一种慢性胃肠道疾病,未来患结肠癌的风险不断增加。细胞凋亡和炎症在该疾病的病因中起重要作用。微小RNA与包括IBD在内的不同疾病的病因相关。在本研究中,我们旨在探讨miR-135a在葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠模型中结肠炎病因中的作用。
结果显示,结肠细胞中miR-135a的表达受到抑制,上调miR-135a可抑制结肠上皮细胞的凋亡和炎症。此外,缺氧诱导因子1α(Hif1α)被鉴定为miR-135a的靶基因,其促进细胞凋亡和炎症,因为敲低Hif1α会导致细胞凋亡和炎症均受到抑制。
由于miR-135a在体外具有抗凋亡和抗炎作用,其过表达可能对IBD有益。