RTCB deficiency triggers colitis in mice by influencing the NF-κB and Wnt/β-catenin signaling pathways  

作　　者：Peiyan Liu Ruitao Zhang Xiaotong Song Xiaohua Tian Yichao Guan Licheng Li Mei He Chengqiang He Naizheng Ding 

机构地区：[1]College of Life Science,Shandong Normal University,Jinan 250014,China

出　　处：《Acta Biochimica et Biophysica Sinica》2024年第3期405-413,共9页生物化学与生物物理学报（英文版）

基　　金：This work was supported by the grants from the Natural Science Foundation of Shandong Province(Nos.ZR2022MC083 and ZR2020MC081);the National Natural Science Foundations of China(No.31771659).

摘　　要：RNA terminal phosphorylase B(RTCB)has been shown to play a significant role in multiple physiological processes.However,the specific role of RTCB in the mouse colon remains unclear.In this study,we employ a conditional knockout mouse model to investigate the effects of RTCB depletion on the colon and the potential molecular mechanisms.We assess the efficiency and phenotype of Rtcb knockout using PCR,western blot analysis,histological staining,and immunohistochemistry.Compared with the control mice,the Rtcb-knockout mice exhibit compromised colonic barrier integrity and prominent inflammatory cell infiltration.In the colonic tissues of Rtcbknockout mice,the protein levels of TNF-α,IL-8,and p-p65 are increased,whereas the levels of IKKβand IκBαare decreased.Moreover,the level of GSK3βis increased,whereas the levels of Wnt3a,β-catenin,and LGR5 are decreased.Collectively,our findings unveil a close association between RTCB and colonic tissue homeostasis and demonstrate that RTCB deficiency can lead to dysregulation of both the NF-κB and Wnt/β-catenin signaling pathways in colonic cells.

关 键 词：RTCB COLITIS NF-ΚB WNT/Β-CATENIN LGR5 

分 类 号：R574.62[医药卫生—消化系统]