RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways

• Verfasst von: Formoso, Karina [VerfasserIn]
• Verfasst von: Susperreguy, Sebastian [VerfasserIn]
• Verfasst von: Freichel, Marc [VerfasserIn]
• Verfasst von: Birnbaumer, Lutz [VerfasserIn]
• Titel: RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways
• Verf.angabe: Karina Formoso, Sebastian Susperreguy, Marc Freichel & Lutz Birnbaumer
• E-Jahr: 2020
• Jahr: 29 April 2020
• Fussnoten: Gesehen am 17.09.2020
• Titel Quelle: Enthalten in: Scientific reports
• Ort Quelle: [London] : Macmillan Publishers Limited, part of Springer Nature, 2011
• Jahr Quelle: 2020
• Band/Heft Quelle: 10(2020) Artikel-Nummer 7227, 20 Seiten
• ISSN Quelle: 2045-2322
• DOI: doi:10.1038/s41598-020-61177-x
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1733247769

Abstract

The seven-member transient receptor potential canonical genes (TRPC1-7) encode cation channels linked to several human diseases. There is little understanding of the participation of each TRPC in each pathology, considering functional redundancy. Also, most of the inhibitors available are not specific. Thus, we developed mice that lack all of the TRPCs and performed a transcriptome analysis in eight tissues. The aim of this research was to address the impact of the absence of all TRPC channels on gene expression. We obtained a total of 4305 differentially expressed genes (DEGs) in at least one tissue where spleen showed the highest number of DEGs (1371). Just 21 genes were modified in all the tissues. Performing a pathway enrichment analysis, we found that many important signaling pathways were modified in more than one tissue, including PI3K (phosphatidylinositol 3-kinase/protein kinase-B) signaling pathway, cytokine-cytokine receptor interaction, extracellular matrix (ECM)-receptor interaction and circadian rhythms. We describe for the first time the changes at the transcriptome level due to the lack of all TRPC proteins in a mouse model and provide a starting point to understand the function of TRPC channels and their possible roles in pathologies.