Basic & Clinical Medicine ›› 2023, Vol. 43 ›› Issue (6): 941-947.doi: 10.16352/j.issn.1001-6325.2023.06.0941

• Original Articles • Previous Articles     Next Articles

E3 ubiquitinase RNF138 inhibits the development of ulcerative colitis

DENG Boya1, LU Yalan2, YU Si3, ZHANG Yiyao1, HUANG Jingyi3, LI Yue3*, LIU Changzheng1*   

  1. 1. State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences CAMS, School of Basic Medicine PUMC, Beijing 100005;
    2. Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences & Peking Union Medical College; Key Laboratory of Human Disease Comparative Medicine, National Health Commission, Beijing 100021;
    3. Department of Gastroenterology, Peking Union Medical College Hospital, CAMS & PUMC, Beijing 100730, China
  • Received:2023-03-06 Revised:2023-04-18 Online:2023-06-05 Published:2023-05-31
  • Contact: *cz-liu@ibms.pumc.edu.cn;liyue@pumch.cn

Abstract: Objective To explore the role of RNF138 (ring finger protein 138) in the ulcerative colitis (UC). Methods The expression of RNF138 in active, remission and ulcerative colitis upon immunosuppressive treatment was analyzed by GEO database. The UC model was constructed by RNF138-deficient mice. The pathological observation, histological analysis and colon measurement were performed by the model mice. The transcriptome analysis was employed by using mouse colon tissue samples. The expression levels of RNF138 and p-p65 in colon tissue of model mice were detected by immunohistochemistry and Western blots. The expression of target gene of NF-кB pathway was detected by qPCR. Immunohistochemistry was used to evaluate the expression of RNF138 and NF-кB p65 in clinical samples of UC. Results GEO database and clinical samples showed that the expression of RNF138 decreased in the samples of active UC as compared to that in the remission stage(P<0.05). Knocking out RNF138 promoted the occurrence and progression of DSS induced UC (P<0.05). Knocking out RNF138 promoted upregulation of p-p65 and its target gene expression(P<0.05), indicating NF-кB signal pathway activation. Conclusions RNF138 inhibits the development of UC through suppressing the NF-кB genetic pathway.

Key words: RNF138, ulcerative colitis, NF-кB

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