Ameliorating Effects of TRIM67 against Intestinal Inflammation and Barrier Dysfunction Induced by High Fat Diet in Obese Mice

• Published in: International journal of molecular sciences Vol. 23; no. 14; p. 7650
• Main Authors: Luo, Qihui, Jahangir, Asad, He, Junbo, Huang, Chao, Xia, Yu, Jia, Lanlan, Wei, Xiaoli, Pan, Ting, Du, Yanni, Mu, Bin, Gong, Huan, Liu, Wentao, Ur-Rehman, Saif, Pan, Kangcheng, Chen, Zhengli
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 11.07.2022; MDPI
• Subjects: Animals; Apoptosis; Autophagy; Carcinogenesis; Carcinogens; Colon; Cytokines; Cytoskeletal Proteins; Diet; Diet, High-Fat - adverse effects; High fat diet; Ileum; Immune response; In vivo methods and tests; Inflammation; Inflammation - pathology; Inflammatory bowel disease; Intestine; knockout; Metabolic disorders; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Obese; Myc protein; Obesity; Obesity - metabolism; Oxidative stress; Palmitic acid; Permeability; Protein expression; Proteins; Small intestine; Swine; TRIM67; Tripartite Motif Proteins - metabolism; knockout; intestine; inflammation; high fat diet; TRIM67
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23147650

Tripartite Motif 67 (TRIM67) is an important member of TRIM family proteins, which participates in different cellular processes including immune response, proliferation, differentiation, carcinogenesis, and apoptosis. In recent years, a high fat diet (HFD) has remained one of the main causes of different metabolic diseases and increases in intestinal permeability as well as inducing intestinal inflammation. The current study investigated the protective effects of in the ileum and colon of obese mice. 4-week-old wild-type (WT) C57BL/6N mice and knockout (KO) C57BL/6N mice were selected and randomly divided into four sub-groups, which were fed with control diet (CTR) or HFD for 14 weeks. Samples were collected at the age of 18 weeks for analysis. To construct an in vitro obesity model, over-expressed IPEC-J2 cells (porcine intestinal cells) with were stimulated with palmitic acid (PA), and its effects on the expression level of , inflammatory cytokines, and barrier function were evaluated. The KO mice showed pathological lesions in the ileum and colon and this effect was more obvious in KO mice fed with HFD. In addition, KO mice fed with a HFD or CTR diet had increased intestinal inflammation, intestinal permeability, and oxidative stress compared to that WT mice fed with these diets, respectively. Moreover, IPEC-J2 cells were transfected with TRIM67 plasmid to perform the same experiments after stimulation with PA, and the results were found consistent with the in vivo evaluations. Taken together, our study proved for the first time that HFD and KO mice have synergistic damaging effects on the intestine, while plays an important protective role in HFD-induced intestinal damage.