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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Multi-Omics Analysis and Nephroseq Database of Genes Related to Kidney Function in Diabetic Nephropathy Patients to
Ling Deng1, Feifan Yan1, Changmei Feng1
1Department of Endocrinology, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, Guangxi, Zhuang Autonomous Region, 541002, People's Republic of China.
Purpose:
Diabetic nephropathy (DN), a major complication of type 2 diabetes and leading cause of end-stage renal disease, lacks complete molecular understanding. To elucidate the mechanisms underlying kidney injury in DN, we analyzed mRNA and protein expression changes in mouse kidney tissue, aiming to provide a theoretical foundation for drug development.
Methods:
C57BL/6 mice were divided into two groups: a normal control group and a diabetes model group. The type 2 diabetes model was established using a high-fat diet (HFD) combined with streptozotocin (STZ). Fasting blood glucose levels and glucose tolerance tests were performed to evaluate glucose metabolism. Kidney tissues were collected, with the left kidney rapidly frozen in liquid nitrogen for transcriptomic and proteomic analyses, and the right kidney fixed in paraformaldehyde for subsequent preparation of paraffin-embedded blocks and staining.
Results:
Diabetic nephropathy (DN) mice showed significant transcriptomic and proteomic alterations in kidney tissues compared to controls. Transcriptomic analysis revealed 4156 upregulated and 1121 downregulated genes, while proteomic analysis identified 887 differentially expressed proteins (DEPs: 687 upregulated, 200 downregulated). 240 genes were synchronously upregulated and 111 synchronously downregulated at both levels, functionally linked to cellular immunity, autophagy, inflammation, and lipid metabolism. CytoHubba identified 10 hub genes: FN1, TTR, APOA1, ITGB2, APOE, PTPRC, STAT3, VTN, ICAM1, and ANXA2. Nephroseq database analysis of human DN patients showed FN1, STAT3, ICAM1, and ANXA2 were significantly upregulated and APOA1 was significantly downregulated in kidney tissues. Furthermore, FN1, ICAM1, and ANXA2 negatively correlated with eGFR, while APOA1 positively correlated with eGFR.
Conclusion:
Diabetic mice exhibited varying degrees of pathological changes in the kidneys. Combined transcriptomic and proteomic analyses highlighted four genes-FN1, ICAM1, ANXA2, and APOA1-as potential therapeutic targets for improving diabetic nephropathy.
Insights
This study investigated molecular changes in diabetic nephropathy (DN) using combined transcriptomic and proteomic analyses in mice. Four key genes (FN1, ICAM1, ANXA2, APOA1) were identified as potential therapeutic targets for DN.
Area of Science:
- Biochemistry
- Genomics
- Proteomics
Background:
- Diabetic nephropathy (DN) is a severe complication of type 2 diabetes, leading to end-stage renal disease.
- The precise molecular mechanisms driving kidney injury in DN remain incompletely understood.
- Identifying these mechanisms is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying kidney injury in diabetic nephropathy.
- To analyze mRNA and protein expression changes in mouse kidney tissue.
- To provide a theoretical basis for novel drug development targeting DN.
Main Methods:
- Type 2 diabetes model established in C57BL/6 mice using a high-fat diet and streptozotocin.
- Transcriptomic and proteomic analyses performed on kidney tissues.
- Differential gene and protein expression identified and correlated with kidney function markers.
Main Results:
- Significant transcriptomic and proteomic alterations observed in DN mouse kidneys compared to controls.
- Identified 4156 upregulated and 1121 downregulated genes; 887 differentially expressed proteins.
- Highlighted four key genes (FN1, ICAM1, ANXA2, APOA1) as potential therapeutic targets, with specific correlations to eGFR in human DN patients.
Conclusions:
- Combined transcriptomic and proteomic analyses revealed critical molecular pathways in DN.
- Four genes—FN1, ICAM1, ANXA2, and APOA1—emerged as promising therapeutic targets for diabetic nephropathy.
- Further research into these targets could lead to improved treatments for DN.
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