Related Experiment Video
Updated: Feb 20, 2026
Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
Published on: November 10, 2021
RACK1 silencing attenuates renal fibrosis by inhibiting TGF-β signaling
Jie Feng1, Liyi Xie1, Ranran Kong2
1Department of Nephrology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Abstract:
The receptor for activated C-kinase 1 (RACK1) is a member of the WD40-repeat family of proteins and has been reported to be implicated in the development of liver fibrosis. However, the role of RACK1 in renal fibrosis remains unclear. Therefore, in this study, we investigated the effects of RACK1 on transforming growth factor-β1 (TGF-β1)-treated human proximal tubular epithelial cells and aimed to elucidate the possible mechanisms responsible for its anti-fibrotic effects. Our results revealed that RACK1 was highly expressed in the renal fibrotic tissues and TGF-β1-treated HK-2 cells. RACK1 silencing inhibited TGF-β1‑induced α-smooth muscle actin and connective tissue growth factor expression in the HK-2 cells. Furthermore, RACK1 silencing inhibited the expression of phosphorylated Smad3 in the TGF-β1-treated HK-2 cells. To the best of our knowledge, these data demonstrate for the first time the role of RACK1 in renal fibrosis. The present findings indicate that RACK1 silencing attenuates renal fibrosis by suppressing the activation of TGF-β1/Smad3 signaling pathway in HK-2 cells. Thus, RACK1 may serve as a novel regulator of renal fibrosis.
Insights
Receptor for activated C-kinase 1 (RACK1) plays a role in renal fibrosis. Silencing RACK1 in kidney cells reduces fibrosis markers by inhibiting the TGF-β1/Smad3 pathway.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Receptor for activated C-kinase 1 (RACK1) is a WD40-repeat protein family member.
- RACK1 is implicated in liver fibrosis, but its role in renal fibrosis is unknown.
Purpose of the Study:
- Investigate RACK1's effects on transforming growth factor-β1 (TGF-β1)-treated human proximal tubular epithelial cells (HK-2).
- Elucidate the anti-fibrotic mechanisms of RACK1 in renal cells.
Main Methods:
- Studied RACK1 expression in renal fibrotic tissues and TGF-β1-treated HK-2 cells.
- Utilized RACK1 silencing techniques in HK-2 cells.
- Assessed expression of α-smooth muscle actin, connective tissue growth factor, and phosphorylated Smad3.
Main Results:
- RACK1 was highly expressed in renal fibrotic tissues and TGF-β1-treated HK-2 cells.
- RACK1 silencing inhibited TGF-β1-induced expression of α-smooth muscle actin and connective tissue growth factor.
- RACK1 silencing suppressed the activation of the TGF-β1/Smad3 signaling pathway.
Conclusions:
- RACK1 is highly expressed in renal fibrosis and promotes fibrosis in HK-2 cells.
- RACK1 silencing attenuates renal fibrosis by inhibiting the TGF-β1/Smad3 pathway.
- RACK1 may be a novel therapeutic target or regulator for renal fibrosis.
More Related Videos
10:21Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
07:01Delivery of Exogenous Artificially Synthesized miRNA Mimic to the Kidney Using Polyethylenimine Nanoparticles in Several Kidney Disease Mouse Models
Published on: May 10, 2022
Related Concept Videos
01:16TGF - β Signaling Pathway
01:25Antihypertensive Drugs: Direct Renin Inhibitors
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System