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Updated: Dec 31, 2025

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
TRB3 regulates pulmonary interstitial fibrosis through the MAPK signaling pathway
Wencheng Yu1, Xiaoxia Song2, Yaqiu Liu3
1Department of Pneumology, The Affiliated Hospital of Qingdao University Qingdao 266003, Shandong Province, China.
Abstract:
This study aims to investigate the effects of TRB3 on the EMT and MAPK signaling pathways in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. TRB3 adenovirus vector with green fluorescent protein (GFP) and TRB3-siRNA adenovirus vector were constructed for overexpression and down-regulation of TRB3, respectively. The pulmonary fibrosis mouse model was induced by bleomycin, and then treated with adenovirus on the next day. The mice were randomly killed at the 7th (D7), 14th (D14) and 28th (D28) day, respectively. The lung tissues were collected for histopathologic observations, hydroxyproline determination, Immunohistochemistry, western blot and RT-qPCR to detect the expression of TRB3 and EMT-related proteins. Overexpression of TRB3 caused more severe pulmonary fibrosis (P<0.05), while downregulation of TRB3 significantly reduced pulmonary fibrosis (P<0.05). The expression of MAPK pathway-related and EMT-related genes and proteins was markedly upregulated by TRB3 overexpression (P<0.05), but prominently downregulated by TRB3-shRNA (P<0.05). In conclusion, exogenous regulation of TRB3 may have effects on bleomycin-induced pulmonary fibrosis in mice.
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