PUBLICATION
TYRO3 protects podocyte via JNK/c-jun-P53 pathway
- Authors
- Liwen, Z., Song, J., Shi, J., Xu, X., Wang, L., Xiuwen, Z., Hou, Q., Weisong, Q., Chen, Z.
- ID
- ZDB-PUB-230323-44
- Date
- 2023
- Source
- Archives of biochemistry and biophysics 739: 109578 (Journal)
- Registered Authors
- Chen, Zhaohong, Wang, Ling
- Keywords
- Diabetic nephropathy, Podocyte, TYRO3
- MeSH Terms
-
- Animals
- Apoptosis
- Diabetic Nephropathies*/genetics
- Diabetic Nephropathies*/metabolism
- Podocytes*/metabolism
- Signal Transduction
- Tumor Suppressor Protein p53/genetics
- Tumor Suppressor Protein p53/metabolism
- Zebrafish/metabolism
- PubMed
- 36948351 Full text @ Arch. Biochem. Biophys.
Citation
Liwen, Z., Song, J., Shi, J., Xu, X., Wang, L., Xiuwen, Z., Hou, Q., Weisong, Q., Chen, Z. (2023) TYRO3 protects podocyte via JNK/c-jun-P53 pathway. Archives of biochemistry and biophysics. 739:109578.
Abstract
Podocyte injury plays a critical role in diabetic nephropathy (DN). Our previous work demonstrated a protective role of tyrosine-protein kinase receptor TYRO3 in glomerular disease; However, the downstream signaling of TYRO3 remains unclear. Our data showed that genetic ablation of tyro3 in zebrafish recapitulated a nephrotic syndrome phenotype. TYRO3 expression was suppressed by high glucose and TGF-β, which may contribute to decreased TYRO3 expression in progressive DN. Moreover, knockdown of TYRO3 expression with siRNA induced podocytes apoptosis and cytoskeleton rearrangement. Further study revealed that TYRO3 conferred antiapoptotic effects through the activation of JNK/c-jun-P53 in podocytes. Our results revealed a novel signaling module of TYRO3 in podocyte homeostasis, which provides a new molecular insight of TYRO3 effect in podocyte protection.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping