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The effects of WW2/WW3 domains of Smurf2 molecule on TGF‐β signaling and arginase I gene expression
Author(s) -
Ganji Ali,
Roshan Hani Mosayebzadeh,
Varasteh Abdolreza,
Moghadam Malihe,
Sankian Mojtaba
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10446
Subject(s) - arginase , transforming growth factor , downregulation and upregulation , signal transduction , biology , gene expression , gene , smad , microbiology and biotechnology , biochemistry , amino acid , arginine
Smad ubiquitination regulatory factor 2 (Smurf2) consists of multiple WW domains which can interact with Smad7 molecule and inhibit signaling of transforming growth factor‐beta (TGF‐β) cytokine. Arginase I (ArgI) is one of the main products of TGF‐β signaling that plays important roles in tumor escape and airway tissue fibrosis and remodeling in asthma. In this study, the effects of TAT fused to WW2/WW3 (TAT‐WW2/WW3) recombinant protein on TGF‐β signaling and ArgI gene expression were evaluated on J774A.1 cell culture. For this purpose, interaction of TAT‐WW2/WW3 with Smad7, mRNA expression of ArgI, and phosphorylated Smad3 (P‐Smad3) were analyzed in TAT‐WW2/WW3‐treated J774A.1 cell. The results showed interaction of TAT‐WW2/WW3 with Smad7, downregulation of ArgI gene expression ( P < 0.05), and higher amount of P‐Smad3 in the TAT‐WW2/WW3‐treated cells. In conclusion, we suggest that TAT‐WW2/WW3 could interfere with TGF‐β signaling and reduce ArgI gene expression. Since, ArgI has important effects on tissue remodeling in asthma and cancer progression, so these findings could be used to develop a new approach in the treatment of asthma and cancers.