Ishihara Sayaka, Sato Masashi, Miyazaki Haruka, Saito Haruka, Sato Tsuyoshi, Fujikado Noriyuki, Sawai Satoshi, Kotani Ai, Katagiri Koko
Department of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.
Department of Innovative Medical Science, School of Medicine, Tokai University, Isehara, Kanagawa, Japan.
Gastro Hep Adv. 2023 Feb 4;2(4):487-496. doi: 10.1016/j.gastha.2023.01.021. eCollection 2023.
To examine the roles of microRNAs in the development of colitis, we conducted the RNA-sequencing studies using RNA derived from normal and colitogenic CD4+ T cells. Colitogenic CD4 T cells demonstrated the increased expression of miR-150. We focused on the involvement of miR-150 in the colitis.
We crossed miR-150 knockout mice and T-cell-specific Rap1KO mice, which is colitis model mice and spontaneously develop the colitis with tubular adenomas in microbiota-dependent manner.
MiR-150 silencing completely inhibited the expansion of pathogenic Th17 cells and the development of colitis.
MiR-150 is a potential therapeutic target of inflammatory bowel diseases.
为研究微小RNA在结肠炎发展中的作用，我们使用来自正常和致结肠炎CD4 + T细胞的RNA进行了RNA测序研究。致结肠炎CD4 T细胞显示出miR-150表达增加。我们重点研究了miR-150在结肠炎中的作用。
我们将miR-150基因敲除小鼠与T细胞特异性Rap1基因敲除小鼠进行杂交，后者是结肠炎模型小鼠，以微生物群依赖的方式自发发展为伴有管状腺瘤的结肠炎。
miR-150沉默完全抑制了致病性Th17细胞的扩增和结肠炎的发展。
miR-150是炎症性肠病的潜在治疗靶点。
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