Related Experiment Video
Updated: Oct 3, 2026
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
The Effects of M1/M2 Macrophages on the mRNA Expression Profile of Diabetic Glomerular Endothelial Cells
Yining Li1, Weihong Yu2, Mingyue He2
1Center of Organ Transplantation, The Second Xiangya Hospital of Central South University, Changsha, China.
Objectives:
The aim of this study was to explore the effects of M1/M2 macrophages on the mRNA expression profile of glomerular endothelial cells (GECs) treated with advanced glycosylation end products (AGEs).
Methods:
We cocultured M1/M2 macrophages and GECs treated with AGEs. The mRNA expression profile was detected by transcriptome sequencing. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed using the online tool Database for Annotation, Visualization, and Integrated Discovery (DAVID). The expression of differential genes was confirmed using droplet digital PCR and Western blot.
Results:
The results showed that 1,337 genes were significantly changed in M2 cocultured with AGE-treated GECs compared to those of the M1 cocultured with AGE-treated GECs. The KEGG analysis results show that the differentially expressed genes are primarily involved in specific pathways, including the rat sarcoma signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathway. The expression of Braf, Fgfr2, Map3k1, and Mras, which are involved in the MAPK signaling pathway, was downregulated in cocultured M2 with AGE-treated GECs and was consistent with sequencing. Therefore, the cocultured M1/M2 macrophages with AGE-treated GECs can affect the expression of mRNA in GECs, and M2 macrophages via the MAPK signaling pathway may protect GECs from damage by AGEs.
Conclusion:
Coculturing M1/M2 macrophages and GECs treated with AGEs can affect the mRNA expression in GECs. M2 macrophages can inhibit the Braf, Fgfr2, Map3k1, Mras, and p-ERK expression in the MAPK signaling pathway, which may be related to M2 macrophages protecting GECs from damage by AGEs.
Insights
M2 macrophages may protect glomerular endothelial cells (GECs) from advanced glycosylation end products (AGEs) by downregulating MAPK signaling. This study explored macrophage effects on GEC mRNA expression after AGE treatment.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Glomerular endothelial cells (GECs) are susceptible to damage from advanced glycosylation end products (AGEs).
- Macrophages, specifically M1 and M2 subtypes, play critical roles in inflammation and tissue repair.
- Understanding macrophage-GEC interactions is crucial for addressing AGE-induced kidney damage.
Purpose of the Study:
- To investigate the impact of M1 and M2 macrophages on the mRNA expression profile of GECs exposed to AGEs.
- To identify specific molecular pathways involved in these interactions.
Main Methods:
- Co-culture of M1/M2 macrophages with AGE-treated GECs.
- Transcriptome sequencing to analyze mRNA expression profiles.
- Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
- Validation of differential gene expression using droplet digital PCR and Western blot.
Main Results:
- Significant changes in gene expression were observed in GECs co-cultured with M2 macrophages compared to M1.
- Differentially expressed genes were primarily associated with the rat sarcoma (RAS) and mitogen-activated protein kinase (MAPK) signaling pathways.
- Key genes in the MAPK pathway (Braf, Fgfr2, Map3k1, Mras) were downregulated in the M2 co-culture group.
Conclusions:
- M1/M2 macrophages modulate mRNA expression in GECs treated with AGEs.
- M2 macrophages appear to protect GECs from AGE-induced damage, potentially by inhibiting the MAPK signaling pathway.
- Further research into M2 macrophage-mediated protection mechanisms is warranted.
More Related Videos
08:37Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
10:31Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
