title: Knockdown of elF3a inhibits collagen synthesis in renal fibroblasts via Inhibition of transforming growth factor-β1/Smad signaling pathway.
abstract: Renal fibrosis is characterized by an exacerbated accumulation of deposition of the extracellular matrix (ECM). The eukaryotic translation initiation factor (eIF) 3a is the largest subunit of the eIF3 complex and has been involved in pulmonary fibrosis. However, the role of eIF3a in rental fibrosis is still unclear. Therefore, in this study, we investigated the role of eIF3a in rental fibrosis and explored the underlying mechanism. Our study found that eIF3a was up-regulated in renal fibrotic tissues and transforming growth factor (TGF)-β1-treated HK-2 cells. In addition, knockdown of eIF3a significantly inhibited TGF-β1-induced expression levels of α-smooth muscle actin (α-SMA) and collagen I. Furthermore, knockdown of eIF3a attenuated TGF-β1-induced Smad3 activation in HK-2 cells. Taken together, these results suggest that knockdown of eIF3a inhibits collagen synthesis in renal fibroblasts via inhibition of TGF-β1/Smad signaling pathway, and eIF3a may be a potential molecular target for the treatment of renal fibrosis.
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Yun-Fang
authors.initials: YF
authors.lastname: Zhang
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Wang
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Jie
authors.initials: J
authors.lastname: Luo
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Shen
authors.initials: S
authors.lastname: Yang
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Jie-Lin
authors.initials: JL
authors.lastname: Wang
authors.affiliation: Department of Nephrology, Huadu District People's Hospital, Southern Medical University Guangzhou 510800, People's Republic of China.
authors.forename: Hong-Yan
authors.initials: HY
authors.lastname: Li
mesh_terms: D002460:Cell Line; D003094:Collagen / Q000378:metabolism*; D039621:Eukaryotic Initiation Factor-3 / Q000235:genetics* / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism* / Q000473:pathology; D005355:Fibrosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D007674:Kidney Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D015398:Signal Transduction / Q000235:genetics; D051785:Smad Proteins / Q000235:genetics / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: C105988:EIF3A protein, human; D039621:Eukaryotic Initiation Factor-3; D051785:Smad Proteins; D053773:Transforming Growth Factor beta1; D003094:Collagen
keywords: Eukaryotic translation initiation factor (eIF) 3a; TGF-β1; renal fibrosis