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Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
Sivarajan Kumarasamy1, Sumeet Solanki1, Oluwatomisin T Atolagbe1
1Department of Physiology and Pharmacology, and Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine and Life Sciences, University of Toledo Health Science Campus, 3000 Transverse Dr., Toledo, Ohio 43614 USA.
Abstract:
In previous studies using mice with macrophage-specific loss of TRPC3 we found a significant, selective effect of TRPC3 on the biology of M1, or inflammatory macrophages. Whereas activation of some components of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cells, gathering insight about other molecular signatures within macrophages that might be affected by Trpc3 expression requires an alternative approach. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 and their littermate controls. We identified 160 significantly differentially expressed genes between the two groups, of which 62 were upregulated and 98 downregulated in control vs. Trpc3-deficient M1 macrophages. Gene ontology analysis revealed enrichment in processes associated to cellular movement and lipid signaling, whereas the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included networks for calcium signaling and cell adhesion molecules, among others. This is the first deep transcriptomic analysis of macrophages in the context of Trpc3 deficiency and the data presented constitutes a unique resource to further explore functions of TRPC3 in macrophage biology.
Insights
TRPC3 deficiency impacts inflammatory macrophages, altering gene expression related to cell movement and lipid signaling. This study provides a transcriptomic resource for understanding TRPC3's role in macrophage biology.
Area of Science:
- Immunology
- Molecular Biology
- Genomics
Background:
- TRPC3 (Transient Receptor Potential Cation Channel Subfamily C Member 3) plays a role in M1 inflammatory macrophage biology.
- Previous studies indicated TRPC3 affects unfolded protein response and apoptosis mediators (CamkII, Stat1).
- Further investigation into TRPC3's broader molecular impact on macrophages is needed.
Purpose of the Study:
- To comprehensively analyze the transcriptome of M1 macrophages lacking TRPC3.
- To identify novel molecular pathways and gene signatures influenced by TRPC3 deficiency.
Main Methods:
- RNA-sequencing (RNA-seq) was performed on M1 macrophages from TRPC3-deficient mice and littermate controls.
- Differential gene expression analysis was conducted to compare transcriptomes.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were employed.
Main Results:
- 160 significantly differentially expressed genes were identified between control and TRPC3-deficient M1 macrophages.
- 98 genes were downregulated and 62 were upregulated in TRPC3-deficient M1 macrophages compared to controls.
- GO analysis highlighted enrichment in cellular movement and lipid signaling pathways.
- KEGG analysis revealed enrichment in calcium signaling and cell adhesion molecule pathways.
Conclusions:
- This study presents the first deep transcriptomic analysis of macrophages in the context of TRPC3 deficiency.
- The findings reveal TRPC3 influences macrophage gene expression, particularly in cellular movement, lipid signaling, calcium signaling, and cell adhesion.
- The generated data serves as a valuable resource for future research into TRPC3 functions in macrophage biology.
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