Project description:Effects of TRPC1 silencing on whole-transcriptome gene expression were determined in Huh7 hepatocellular carcinoma cells using whole-transcriptome gene expression profiling.
Project description:Effects of TRPC1 silencing on whole-transcriptome gene expression were determined in human primary aortic vascular smooth muscle cells using whole-transcriptome gene expression profiling.
Project description:Muscle growth is a quantitative trait controlled by multiple genes in animals. Previously, we showed that transient receptor potential channel 1 (TRPC1) was a differentially expressed gene in muscle tissues between pig breeds with divergent growth traits using RNA-seq. In this study, we characterized the expression profiles of TRPC1 in different tissues and various pig breeds, and found that TRPC1 is highly expressed in muscle. We found two effective single nucleotide polymorphism (SNP) sites (C-1763T and C-1604T) in TRPC1 that could affect the activity of the promoter region and regulate the growth rate of pigs. Functionally, we used RNAi and overexpression to illustrate that TRPC1 promotes myoblast proliferation, migration, differentiation, fusion, and muscle hypertrophy, while inhibiting muscle degradation, and that these processes may be mediated by activating the Wnt signaling pathways. Taken together, our results revealed that TRPC1 may be a promoter of muscle growth and development and it plays a role in Wnt-mediated myogenesis.
Project description:To investigate the mechanism of TRPC1 or TRPC6 on the regulation of endotoxemic cardiac dysfunction, we established Trpc1-/- and Trpc6-/- mice. LPS-challenged endotoxemic mouse model was built, and the gene expression profile was analyzed using data obtained from RNA-seq of WT, LPS-challenged WT, LPS-challenged Trpc1-/-, and LPS-challenged Trpc6-/- mice hearts.
Project description:Transient receptor potential channel 1 (TRPC1) is a widely expressed mechanosensitive ion channel located within the endoplasmic reticulum membrane, crucial for refilling depleted internal calcium stores during activation of calcium-dependent signaling pathways. Here, we have demonstrated that TRPC1 activity is protective within cartilage homeostasis in the prevention of cellular senescence associated cartilage breakdown during mechanical and inflammatory challenge. We revealed that TRPC1 loss is associated with early stages of osteoarthritis (OA) and plays a non-redundant role in calcium signaling in chondrocytes. Trpc1-/- mice subjected to destabilization of the medial meniscus induced OA developed a more severe OA phenotype than wild type controls. During early OA development, Trpc1-/- mice displayed an increased chondrocyte survival rate, however remaining cells displayed features of senescence including p16INK4a expression and decreased Sox9. RNA sequencing identified differentially expressed genes related to cell number, apoptosis and extracellular matrix organization. Trpc1-/- chondrocytes exhibited accelerated dedifferentiation, while demonstrating an increased susceptibility to cellular senescence. Targeting the mechanism of TRPC1 activation may be a promising therapeutic strategy in osteoarthritis prevention.
Project description:Investigation of whole genome gene expression level changes in TRIB3-silenced MCF7 cells as compared to Control MCF7 cells. Analysis of activity changes of pathways for FOXO1 phosphorylation between TRIB3-silenced and Control MCF7 cells.