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- 저자 : Yinglei Miao (검색결과 2 건)
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Yunzhen Zhu,Juan Luo,Zhaoqing Yang,Yinglei Miao 한국유전학회 2020 Genes & Genomics Vol.42 No.10
Background Previous investigations reported that the imbalance of intestinal microfora may be the initiation and promotion factor in the pathogenesis of infammatory bowel disease such as ulcerative colitis (UC). Glucocorticoid is a very important class of regulatory molecules in the body. The response of diferent individuals to glucocorticoids can be divided into glucocorticoid sensitive, glucocorticoid resistance and glucocorticoid dependence. Objective We aimed to investigate the diferences in intestinal microfora composition and related metabolic pathways in UC patients with these three diferent glucocorticoid response types. Methods The whole genomic DNA was extracted from fecal specimens. High-throughput sequencing technology was used to analyze the fecal 16S rRNA genome of UC patients with diferent glucocorticoid response types, and functional prediction was performed by PICRUSTs software. Results The results showed that the intestinal microfora of the three groups were mainly composed of Firmicutes, Proteobacteria and Bacteroidetes. Although the species abundance and diversity of intestinal microfora in UC patients difered little among the three groups, the composition of intestinal microfora showed signifcant heterogeneity, which directly led to diferences in the function of intestinal microbiota of UC patients with diferent glucocorticoid responses. Furthermore, of the 240 pathways, “PANTO-PWY: phosphopantothenate biosynthesis I”, “COA-PWY-1: coenzyme A biosynthesis II (mammalian)” and “PWY-4242: pantothenate and coenzyme A biosynthesis III” were signifcantly diferent in the three groups. Conclusions These results indicate that UC patients with diferent glucocorticoids response types have diferent bacterial compositions and functions, which lays a foundation for further study of glucocorticoid resistance in UC patients.
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Keratin 1 maintains the intestinal barrier in ulcerative colitis
Jing Wu,Junkun Niu,Maojuan Li,Yinglei Miao 한국유전학회 2021 Genes & Genomics Vol.43 No.12
Background The intestinal mechanical barrier plays a key role in the pathogenesis of ulcerative colitis (UC). Our previous study showed keratin 1 (KRT1) was downregulated in UC, but the mechanism by which KRT1 afects the intestinal barrier remains unknown. Objectives To explore the mechanism of KRT1 in the intestinal barrier in UC. Methods Colonic tissues were collected from 20 UC patients before and after mucosal healing (MH) and 15 healthy controls. The expression of KRT1 was measured by PCR, western blotting and immunohistochemistry (IHC). A dextran sulfate sodium (DSS)-induced colitis model was established in krt1 transgenic (TG) mice, and the mice were treated with methylprednisolone (MP) to explore the role of KRT1 in the intestinal barrier. Infammation was evaluated through the DAI score, colon, spleen and H&E. The expression of KRT1 and tight junction (TJ) proteins in mouse was analysed by the same methods. Results The transcription and expression of KRT1 in UC was decreased and recovered after MH but did not reach the level of the healthy controls. Similar to the clinical results, the expression of krt1 was decreased in DSS-induced colitis and upregulated after MP. Moreover, the krt1 TG group exhibited less infammation than wild-type (WT) group. The expression of Occludin and ZO-1 decreased after DSS induction, the decreases in Occludin and ZO-1 in the krt1 TG group were lower than WT group, which was signifcantly increased after MP, while the expression of Claudin-2 exhibited the opposite efect. Conclusions Keratin 1 maintains the intestinal barrier by upregulating TJ proteins in UC.
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