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Differential expression profile analysis of PSTK-regulated mRNAs in podocytes
Dong Zheng1, Ying Zhao1, Limin Liu1
1Department of Pathology and Pathophysiology, Medical College of Soochow University, Suzhou, Jiangsu, China.
Abstract:
This study aimed to elucidate the precise mechanisms underlying the protective effects of phosphoseryl-tRNA kinase (PSTK) against cisplatin-induced podocyte injury. PSTK overexpression and knockdown vectors were generated and transfected into murine podocyte cells-5. PSTK levels were measured, and transcriptome sequencing was conducted. Differential expression analysis was performed to identify messenger RNAs (mRNAs) that were positively and negatively correlated with PSTK. We selected 10 candidate genes identified via real-time quantitative polymerase chain reaction and Western blot analysis for further analysis. As expected, PSTK levels were significantly higher in PSTK-overexpressing podocytes and significantly lower in PSTK-knockdown podocytes. PSTK overexpression resulted in the upregulation of 122 genes and downregulation of 372 genes in podocytes. On the other hand, PSTK knockdown resulted in the upregulation of 231 genes and downregulation of 445 genes. Furthermore, the analysis revealed that 11 genes were positively correlated with PSTK, whereas 20 genes were negatively correlated with PSTK. The obtained PSTK-regulated genes were primarily involved in molecular function, biological process, and cellular component, as well as the angiogenesis pathway. The Wnt family member 10A levels were significantly higher after PSTK overexpression, but were significantly lower after PSTK knockdown. In addition, Na+/K+ ATPase subunit α-2 and matrix metalloproteinase 9 levels were significantly downregulated after PSTK overexpression, but significantly upregulated upon PSTK knockdown. Cell proliferation was significantly increased upon PSTK overexpression, but significantly decreased upon PSTK suppression. The results of this study not only identified several significant PSTK-regulated genes for further validation, but also provided insights into the mechanisms underlying the protective effects of PSTK on podocytes.
Insights
Phosphoseryl-tRNA kinase (PSTK) protects against cisplatin-induced podocyte injury by regulating gene expression, including Wnt10a, MMP9, and Na+/K+ ATPase. PSTK influences cell proliferation and angiogenesis pathways, offering insights into kidney protection.
Area of Science:
- Nephrology
- Molecular Biology
- Genomics
Background:
- Podocyte injury is a key factor in kidney disease progression.
- Cisplatin is a nephrotoxic chemotherapy agent that causes podocyte damage.
- The protective role of phosphoseryl-tRNA kinase (PSTK) in podocyte injury requires further mechanistic elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms by which PSTK exerts protective effects against cisplatin-induced podocyte injury.
- To identify genes and pathways regulated by PSTK in podocytes.
- To understand the impact of PSTK on podocyte function and proliferation.
Main Methods:
- Generation and transfection of PSTK overexpression and knockdown vectors in murine podocyte cell line.
- Measurement of PSTK levels.
- Transcriptome sequencing and differential gene expression analysis.
- Validation of candidate genes using real-time quantitative polymerase chain reaction and Western blot analysis.
- Assessment of cell proliferation.
Main Results:
- PSTK overexpression upregulated 122 genes and downregulated 372 genes; PSTK knockdown upregulated 231 genes and downregulated 445 genes.
- 11 genes were positively correlated with PSTK, and 20 genes were negatively correlated.
- PSTK-regulated genes are involved in molecular function, biological processes, cellular components, and the angiogenesis pathway.
- Wnt family member 10A, Na+/K+ ATPase subunit α-2, and matrix metalloproteinase 9 levels were significantly altered by PSTK modulation.
- PSTK overexpression increased cell proliferation, while PSTK suppression decreased it.
Conclusions:
- PSTK plays a significant role in regulating gene expression in podocytes, impacting pathways crucial for kidney function.
- PSTK influences key genes involved in cell signaling, matrix remodeling, and ion transport.
- The findings provide novel insights into the protective mechanisms of PSTK against podocyte injury and suggest its therapeutic potential in kidney diseases.
