The effects of serotonin by Tph1 and Htr2b on skeletal muscle
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1153381 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30467585_1.fastq.gz | Fastqsanger.gz | |||
| SRR30467585_2.fastq.gz | Fastqsanger.gz | |||
| SRR30467586_1.fastq.gz | Fastqsanger.gz | |||
| SRR30467586_2.fastq.gz | Fastqsanger.gz | |||
| SRR30467587_1.fastq.gz | Fastqsanger.gz |
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Project description:It is known that reducing circulating serotonin by inhibiting Tph1 increases the sensitivity of BAT cells and this drives thermogenesis by fat and glucose oxidation. In our results inhibiting Tph1 in muscle showed activation of SIRT1/LKB1/AMPK pathway in skeletal muscle cells and increased p-ACC. Also, it's known that inhibiting adipose Htr2b signaling ameliorates HFD-induced systemic insulin resistance. Here we report insulin sensitivity changes by regulating serotonin in skeletal muscle by Htr2b. Inhibiting Htr2b increases AMPK activity, glucose uptake, and myofiber size and decreases lipid droplet accumulation in HFD mice skeletal muscle. These results indicate improved insulin resistance and myosteatosis in skeletal muscle by lack of Serotonin by Tph1/Htr2b on skeletal muscle.
2024-08-29 | GSE275857 | GEO
Project description:Reducing circulating serotonin by inhibition of Tph1 increases the sensitivity of BAT cells and this drives thermogenesis by fat and glucose oxidation. Here we report Insulin sensitivity changes by regulating Serotonin on skeletal muscle. Improved glucose tolerance and insulin sensitivity in HFD Tph1 KO mice. Inhibiting Tph1 increases AMPK activity, glucose uptake, myofiber size and decreases lipid droplet accumulation in HFD mice skeletal muscle. Inhibiting Tph1 in muscle showed activation of SIRT1/LKB1/AMPK pathway in skeletal muscle cells and increased p-ACC. Theses results indicates that protected insulin resistance and myosteatosis on skeletal muscle by lack of Serotonin by Tph1 on skeletal muscle.
2024-10-17 | GSE279210 | GEO
Project description:The effects of serotonin by Tph1 on skeletal muscle
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Project description:Serotonin is important material in our body. 5-HT is synthesized by TPH1 starting with tryptophan and this compound exists on colorectal cancer. And serotonin combines with various receptors to conduct the metabolic pathway in colorectal cancer. Each receptor relates with various metabolism, such as lipid metabolism, growth, immunity, etc. In this way, medicine which inhibits these receptors can expect for therapy of colorectal cancer. Especially HTR 2B has correlation with growth factor and using the inhibitor of HTR2B, SB204741, can have effect on metabolic pathway in colorectal cancer. So, we set the hypothesis that HTR2B antagonist can have negative effect on growth of colorectal cancer.
2024-03-12 | GSE260979 | GEO
Project description:Tryptophan hydroxylase 1 (TPH1), the rate-limiting enzyme in peripheral serotonin biosynthesis, has emerged as a critical driver of neuroendocrine prostate cancer (NEPC) progression. Elevated TPH1 expression is observed in NEPC cell lines and patient tumor samples. To elucidate the role of TPH1 in prostate cancer development and progression, we performed RNA sequencing (RNA-seq) in prostate cancer cells with either TPH1 knockdown or overexpression, compared to respective control cells. Differential gene expression analysis and subsequent pathway enrichment revealed key molecular programs regulated by TPH1. Functionally, TPH1 overexpression promotes tumor cell proliferation and the acquisition of neuroendocrine features, while genetic or pharmacological inhibition of TPH1 suppresses NEPC cell growth and neuroendocrine marker expression. These findings underscore the oncogenic role of TPH1 in NEPC and support its potential as a therapeutic target.
2026-05-22 | GSE302430 | GEO
Project description:Brain myeloid cells, including infiltrating monocyte-derived macrophages (MDMs) and resident microglia play critical roles in regulating debris clearance following ischemic brain injury, shaping neuroinflammation evolution and neurological outcome, yet the underlying mechanism remains elusive. In this study, using single-cell RNA sequencing and fate mapping, we identified serotonin receptor Htr2b+ MDMs as a pivotal subgroup involved in resolving neuroinflammation within the ischemic penumbra. In addition, we find significant accumulation of Htr2b+ MDMs with enhanced phagocytosis and inflammation-resolving gene signatures in the peri-infarct region. Mechanistically, Htr2b activation promotes nuclear translocation of Tfe3, a key lysosomal regulator, enhancing lysosomal biogenesis and supporting sustained phagocytic activity. Myeloid-specific Htr2b ablation impairs debris clearance, exacerbates neuroinflammation and ischemic injury, while pharmacological Htr2b agonism or Tfe3 activation restores the lysosomal competence of brain MDMs and improves post-stroke neurological outcome. In conclusion, we demonstrate a novel Htr2b+ MDM subset that integrates serotonin signaling to license their intrinsic phagocytosis function, alleviating ischemic brain injury.
2026-07-04 | PXD074993 | Pride
Project description:Background: Aortic Stenosis (AS) is a highly prevalent disease involving physiological and structural remodeling of aortic valve, yet lacks effective medical therapy to halt its progression. Serotonin (5HT) signaling has been implicated in valvular disease. We hypothesized that AS is associated with impaired 5HT clearance due to reduced serotonin receptor (SERT) expression and increased 5HT receptor (HTR) activity. Methods: Sixty-six patients with severe AS undergoing aortic valve (AV) replacement were enrolled in the study, and samples from their explanted AV were harvested. Anatomically normal control AVs were obtained from transplant donors. Explanted AVs were collected for gene expression analysis and 5-HTTLPR genotyping. Gene expression was assessed by RT2-profiler gene array. In vivo, 8-week-old mice received 28-day Angiotensin-II (AngII) infusions ± HTR2B antagonist (LY272015) through subcutaneous Alzet osmotic-pump implants. AV structure and function were assessed via echocardiography, histology, and RNA sequencing. Human aortic valve interstitial cells (AVICs) were treated with either H2O2 or AngII ± SERT siRNAs to assess 5HT signaling and fibrotic/osteogenic markers. Results: AS patients exhibited reduced SERT and increased HTR expression. Oxidative stress in cultured human AVICs suppressed SERT and induced HTR2B expression. AngII ± SERT siRNA promoted VIC osteogenic marker expression. In mice, AngII caused AV thickening, increased velocities and gradients, and activation of fibrosis and calcification-related gene sets, including serotonin, TGFβ, Wnt/β-catenin, PI3K/Akt, and Notch pathways. Pharmacological inhibition of HTR2B preserved AV structure, normalized transvalvular velocities and pressure gradients, and reversed AngII-induced transcriptional changes. Conclusions: In human and mouse AVs, reduced SERT and elevated HTR2B signaling contribute to early-onset fibro-calcific remodeling. HTR2B inhibition by LY272015 reverses these effects, suggesting it as a potential therapeutic strategy for AS.
2026-03-01 | GSE318212 | GEO
Project description:Serotonin in the mammary gland is known to regulate processes such as calcium homeostasis, tight junction permeability, and milk protein gene expression. The objective of this study was to discover novel genes, pathways and functions which serotonin modulates during lactation. The rate-limiting enzyme in the synthesis of non-neuronal serotonin is tryptophan-hydroxylase (TPH1). Therefore, we used TPH1 knock-out mice dams (serotonin deficient) and compared them to wild-type dams and also Tph1 deficient dams injected daily with 5-HTP. Mammary gland tissues were collected on day 10 of lactation and then analyzed by RNA sequencing. Genome-wide gene expression profiles of 12 mouse mammary gland samples were evaluated using RNA sequencing; these 12 samples belong to wild-type dams (WT; n = 4), Tryptophan hydroxylase (Tph1) knock-out dams (KO; Tph1 deficient; n = 4), and Tph1 deficient dams injected daily with 5-HTP (RC; n = 4). Mammary tissues were collected on day 10 of lactation and then underwent RNA extraction, library generation, and subsequent sequencing.
2015-04-28 | E-GEOD-68315 | biostudies-arrayexpress
Project description:Serotonin in the mammary gland is known to regulate processes such as calcium homeostasis, tight junction permeability, and milk protein gene expression. The objective of this study was to discover novel genes, pathways and functions which serotonin modulates during lactation. The rate-limiting enzyme in the synthesis of non-neuronal serotonin is tryptophan-hydroxylase (TPH1). Therefore, we used TPH1 knock-out mice dams (serotonin deficient) and compared them to wild-type dams and also Tph1 deficient dams injected daily with 5-HTP. Mammary gland tissues were collected on day 10 of lactation and then analyzed by RNA sequencing.
2015-04-28 | GSE68315 | GEO
Project description:Monocyte-derived liver macrophages are critical in the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) and liver fibrosis, but their recruitment mechanisms remain unclear. Serotonin (5-hydroxytryptamine, 5HT) is a conserved monoamine synthesized by tryptophan hydroxylase (Tph) 1 in peripheral tissues and Tph2 in the brain. We show that in mice housed at thermoneutrality and fed a high-fat, high-fructose diet, inhibition of peripheral serotonin (pe5HT) through genetic deletion of Tph1 prevents MASH independently of reductions in body weight. Liver flow cytometry and single-nuclei sequencing showed reduced pro-inflammatory Ly6Chigh monocytes, monocyte-derived Kupffer cells (moKCs), and lipid-associated macrophages (LAMs) in Tph1 KO mice. Tph1 deletion also decreased circulating monocytes, specifically Ly6Chigh monocytes. A single 5HT injection increased Ly6Chigh monocytes, while Tph1 KO mice had reduced monocytes without affecting bone marrow monocytes. Mechanistically, serotonin inhibition increases liver AMPK activity, and this is important for reducing CCL2 and monocyte recruitment. These findings link two ancient energy sensors, 5HT and AMPK, with obesity-associated liver fibrosis.
2025-10-30 | E-MTAB-15760 | biostudies-arrayexpress