Function of the porcine TRPC1 gene in myogenesis and muscle growth
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA675023 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12999051_1.fastq.gz | Fastqsanger.gz | |||
| SRR12999051_2.fastq.gz | Fastqsanger.gz | |||
| SRR12999052_1.fastq.gz | Fastqsanger.gz | |||
| SRR12999052_2.fastq.gz | Fastqsanger.gz | |||
| SRR12999053_1.fastq.gz | Fastqsanger.gz |
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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.
2020-11-07 | GSE160972 | GEO
Project description:In animals, muscle growth is a quantitative trait controlled by multiple genes. Previously, we showed that the transient receptor potential channel 1 (TRPC1) gene was differentially expressed in muscle tissues between pig breeds with divergent growth traits base on RNA-seq. Here, we characterized TRPC1 expression profiles in different tissues and pig breeds and showed that TRPC1 was highly expressed in the muscle. We found two single nucleotide polymorphisms (SNPs) (C-1763T and C-1604T) in TRPC1 that could affect the promoter region activity and regulate pig growth rate. Functionally, we used RNAi and overexpression to illustrate that TRPC1 promotes myoblast proliferation, migration, differentiation, fusion, and muscle hypertrophy while inhibiting muscle degradation. These processes may be mediated by the activation of Wnt signaling pathways. Altogether, our results revealed that TRPC1 might promote muscle growth and development and plays a key role in Wnt-mediated myogenesis.
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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.
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Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is commonly used in the treatment of hormone-responsive cancers. The effects of tamoxifen in anabolic tissues harboring estrogen-receptors, such as skeletal muscle, are poorly understood. As estrogen and estrogen receptors play an important role in skeletal muscle development and repair, we hypothesize that tamoxifen may have specific effects on myogenesis, the developmental process underlying muscle cells differentiation and repair. Myogenesis is characterized by fine-tuned changes in protein expression as embryonic myoblasts and adult satellite cells transition from pluripotent stem cells to multinucleated, contractile muscle fibers: we undertake a quantitative proteomic analysis of tamoxifen-induced changes in developing skeletal muscle cells which we expect may also shed light on the effect of tamoxifen on muscle repair.
We report a tandem mass-tag (TMT) approach to tamoxifen-treated myogenesis in C2C12 cells, a well-characterized model of in vitro murine skeletal muscle differentiation. A longitudinal analysis of >10,000 proteins identified in C2C12 myogenesis revealed a novel subset of 1,239 myogenically-regulated proteins. This set of regulatory proteins clustered into five distinct longitudinal expression trends which significantly overlap those obtained in similar analyses performed in human myocytes. A longitudinal analysis of myogenesis in the presence of tamoxifen, when contrasted with a similar analysis in untreated myogenesis finds that while the vast majority of myogenically-regulated proteins were unaffected by tamoxifen treatment, specific pathways and networks are affected. We document a specific functional enrichment for adiponectin-signaling, whereby a set of 198 proteins were differentially expressed relative to controls at one or more stages of myogenesis, the majority of which were involved in steroid biosynthesis, lipid storage and/or metal ion homeostasis. Interestingly, the only protein that was differentially expressed in the tamoxifen-treated cells at every stage of myogenesis was metallothionein-1 (MT1). Elevated levels of MT1 have been correlated with tamoxifen resistance and increased patient mortality and relapse in breast cancer, as well as with cachexia and muscle atrophy in rodent models. Increased MT1 expression levels may contribute to the musculoskeletal effects reported by patients undergoing tamoxifen treatment. Finally, we present a powerful, self-validating pipeline for analyzing the total proteomic response to in vitro treatment across every stage of muscle cells development which can be easily adapted to study the effects of other drugs on myogenesis.
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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.
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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.
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Project description:During muscle differentiation, myogenesis sepcific genes are differentially regulated, including Lamins that function at least in maintenance of nuclear architecture and regulation of gene expression. We used microarrays to detail the global changes of gene expression in lamins and nuclear envelope assoicated proteins during myogenesis. Keywords: comparative, myogenesis
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Project description:Porcine latissimus dorsi muscle is one of the main sources of pork products. Meat quality indicators such as the proportion of muscle fibres within the latissimus dorsi muscle and intramuscular fat deposition change during the growth and development of pigs.We used single-nucleus sequencing (snRNA-seq) to analyse the changes occurring in the longest dorsal muscles of pigs at different growth stages
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