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Upregulation of COL3A1 is a Key Driver in Kidney Stone Formation
Hua Jiang1, Yanji Jiang2, Jie Ji2
1Department of Urology, Affiliated Zhongda Hospital of Southeast University, 210009 Nanjing, Jiangsu, China.
Background:
Kidney stones are a globally prevalent condition, but their pathogenesis remains incompletely understood. This study aimed to identify and validate key genes implicated in kidney stone formation through sequencing data analysis, offering novel molecular targets for elucidating the underlying pathogenic mechanisms.
Methods:
A mouse model of kidney stones was established, and perinephrolithic renal tissue samples were obtained from patients who underwent nephrectomy due to renal dysfunction caused by kidney stones. Transcriptome sequencing was employed to identify differentially expressed genes (DEGs) common to both human and mouse samples. Expression of DEGs in kidney stone specimens was validated using real-time quantitative polymerase chain reaction (qRT-PCR), western blotting, and immunofluorescence (IF). Concurrently, Gene Ontology (GO) and Kyoto Kncyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to investigate functional and pathway associations of the DEGs.
Results:
Transcriptome sequencing identified eight genes consistently upregulated in both humans and mice: COL3A1, TYROBP, MMP2, BASP1, COL5A1, ITGAX, C1QC, and S100A8. qRT-PCR results demonstrated elevated mRNA levels of C1QC and COL3A1 in the perinephrolithic renal tissues of the mouse model. Western blotting confirmed upregulation of COL3A1 at the protein level, and IF staining further verified the specific enrichment of COL3A1 in the renal tissues of the mouse kidney stone model. GO and KEGG enrichment analyses revealed significant associations between the DEGs and immune-related signaling pathways, as well as biological processes involved in extracellular matrix (ECM) remodeling.
Conclusions:
These findings suggest that the ongoing upregulation of COL3A1 could be a key factor in the pathogenesis of kidney stone. Functional enrichment analyses indicate that COL3A1 may promote stone deposition and progression by regulating ECM remodeling and the immune response . These results provide new insights into the molecular mechanisms underlying kidney stone formation.
Insights
Collagen type III alpha 1 chain (COL3A1) upregulation is a key factor in kidney stone formation. This gene influences extracellular matrix remodeling and immune response, offering new molecular targets for kidney stone disease.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Kidney stones are a global health issue with unclear causes.
- Understanding the molecular basis of kidney stone formation is crucial for developing new treatments.
Purpose of the Study:
- To identify and validate key genes involved in kidney stone pathogenesis.
- To explore novel molecular targets for kidney stone disease.
Main Methods:
- Comparative transcriptome sequencing of human and mouse kidney stone tissues.
- Validation of differentially expressed genes (DEGs) using qRT-PCR, western blotting, and immunofluorescence.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
Main Results:
- Eight genes, including COL3A1, were consistently upregulated in human and mouse kidney stone models.
- COL3A1 showed increased mRNA and protein levels in kidney stone tissues.
- DEGs were significantly associated with extracellular matrix remodeling and immune response pathways.
Conclusions:
- Upregulation of COL3A1 is a potential key driver in kidney stone pathogenesis.
- COL3A1 may promote stone formation by influencing ECM remodeling and immune responses.
- These findings offer new molecular insights into kidney stone development.
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