Deep transcriptomic profiling of M1 macrophages lacking Trpc3

• Autores: Kumarasamy, Sivarajan; Solanki, Sumeet; Atolagbe, Oluwatomisin T.; Joe, Bina; Birnbaumer, Lutz; Vazquez, Guillermo
• Año de publicación: 2017
• Idioma: inglés
• Tipo de recurso: artículo
• Fuente: Scientific Reports. 2017;7:39867
• Materia: SISTEMA INMUNOLOGICO; LIPIDOS; MARCADORES BIOLOGICOS; BIOLOGIA CELULAR
• Institución: Pontificia Universidad Católica Argentina

Fil: Kumarasamy, Sivarajan. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos
Fil: Solanki, Sumeet. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos
Fil: Atolagbe, Oluwatomisin T. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos
Fil: Joe, Bina. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Laboratory of Neurobiology; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Vazquez, Guillermo. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos
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.