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Serotonin attenuates tumor-necrosis-factor-alpha-induced intestinal inflammation by interacting with human mucosal tissue

ABSTRACT: Serotonin attenuates tumor-necrosis-factor-alpha-induced intestinal inflammation by interacting with human mucosal tissue

PROVIDER: PRJNA1120458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29299119.fastq.gz	Fastqsanger.gz
	SRR29299120.fastq.gz	Fastqsanger.gz
	SRR29299121.fastq.gz	Fastqsanger.gz
	SRR29299122.fastq.gz	Fastqsanger.gz
	SRR29299123.fastq.gz	Fastqsanger.gz

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Similar Datasets

Serotonin attenuates tumor-necrosis-factor-alpha-induced intestinal inflammation by interacting with human mucosal tissue

Project description:The intestine houses the largest immune system and is serviced by the largest and most complex peripheral nervous system in the human body. The gut-brain axis orchestrates communication between the central and enteric nervous systems, playing a pivotal role in regulating overall body function and intestinal homeostasis. Using a human 3D in vitro model, we investigated the effect of serotonin, a neuromodulator produced in the gut, on immune cell and intestinal tissue interactions. Our findings revealed that serotonin attenuates the tumor-necrosis-factor-alpha-induced pro-inflammatory response, mostly by affecting the expression of chemokines. Serotonin was found to impact tissue-migrating monocytes’ phenotype and distribution, without direct contact with the cells, by remodeling the intestinal tissue. Collectively, using fully human model of intestine, our results show that serotonin has a crucial role in communication among gut-brain axis components and regulates monocyte migration and plasticity, thereby contributing to gut homeostasis and the progression of intestinal inflammation. In vivo studies focused on role of neuromodulators in gut homeostasis and inflammation have shown controversial results, highlighting importance of development of human experimental models. Moreover, our results emphasize importance of human health research in human-cell-based models and suggests serotonin signaling pathway as new therapeutic target for inflammatory bowel disease.

2025-03-12 | GSE269175 | GEO

Serotonin attenuates tumor necrosis factor-induced intestinal inflammation by interacting with human mucosal tissue.

Project description:The intestine hosts the largest immune system and peripheral nervous system in the human body. The gut‒brain axis orchestrates communication between the central and enteric nervous systems, playing a pivotal role in regulating overall body function and intestinal homeostasis. Here, using a human three-dimensional in vitro culture model, we investigated the effects of serotonin, a neuromodulator produced in the gut, on immune cell and intestinal tissue interactions. Serotonin attenuated the tumor necrosis factor-induced proinflammatory response, mostly by affecting the expression of chemokines. Serotonin affected the phenotype and distribution of tissue-migrating monocytes, without direct contact with the cells, by remodeling the intestinal tissue. Collectively, our results show that serotonin plays a crucial role in communication among gut-brain axis components and regulates monocyte migration and plasticity, thereby contributing to gut homeostasis and the progression of inflammation. In vivo studies focused on the role of neuromodulators in gut inflammation have shown controversial results, highlighting the importance of human experimental models. Moreover, our results emphasize the importance of human health research in human cell-based models and suggest that the serotonin signaling pathway is a new therapeutic target for inflammatory bowel disease.

| S-EPMC11873120 | biostudies-literature

Hyperactive Mouse Serotonin Transporter Interacting Proteins LC-MSMS

Project description:The serotonin (5-HT) transporter (SERT) is a key determinant of the concentration of 5-HT available for synaptic signaling and is the target of the antidepressant-selective 5-HT reuptake inhibitors (SSRIs). In addition to the role of SERT in mediating the actions of antidepressant medications, multiple, rare gain of function coding variants in SERT have been identified in subjects with autism spectrum disorder (ASD). The Blakely lab has extensively characterized the structural and functional impact of one of these variants, SERT Ala56, in vitro and in vivo, revealing a constitutively-imposed, biased conformation that enhances transporter function and that perturbs transporter regulation. We hypothesize that SERT Ala56 disrupts the interactions of molecular networks that normally ensure proper transporter structure, localization and regulation, and whose elucidation may reveal new determinants of serotonergic dysfunction in ASD. Here, we pursue an unbiased proteomic analysis of changes in SERT interacting protein (SIPs) imposed by the SERT Ala56 variant, expressed in transgenic mice. Further investigation of the SIPs and associated networks nominated through our studies may provide new opportunities to detect and modulate brain networks that contribute to the underlying complexity of ASD.

2020-05-29 | PXD018695 | Pride

The serotonin transporter is a regulator of neurodegeneration and axon regeneration after retinal injury

Project description:Loss of specialized neurons in neurodegenerative diseases and after nerve injury is mediated in a neuronal subtype- and region-specific fashion. However, little is known about what molecular contexts define selective vulnerability. Here, we demonstrate that retinal ganglion cells (RGCs) in the mouse peripheral ventrotemporal (VT) retina are the most susceptible to optic nerve injury. Mechanistically, we show that the ventral-specific molecule, the serotonin transporter (SERT) is upregulated on VT axons within one day after injury and loss of SERT attenuates VT RGC death and promotes axon regeneration. From RNA-seq analysis, the transmembrane protein Gpnmb has been identified as a target downregulated by SERT. Moreover, GPNMB is involved in RGC protection and axon regeneration. Together, our studies reveal the serotonin transporter as a determinant of selective vulnerability.

2020-07-11 | GSE153812 | GEO

Expression Profile of Embryonic Stem Cell Derived Serotonin Neurons

Project description:The rhesus embryonic stem cell line 366.4 differentiates into serotonin neurons. RNA was extracted from ESC colonies, embryoid body (Ebs), Neurospheres in selection (N1), Proliferating serotonin neurons (N2) and differentiating serotonin neurons (N3). RNA was labeled with Enzo biotin labelling kit and hybridized to Rhesus chip from Affymetrix. single sample represent each stages and total 5 rhesus chip were hybridized

2010-04-08 | E-GEOD-16168 | biostudies-arrayexpress

Serotonin effect on Bxpc-3 pancreatic adenocarcinoma cell line.

Project description:Analysis of Bxpc-3 cells treated with serotonin under metabolic stress induced by serum deprivation. Serotonin (5-HT), a well-known neuromodulator with both neurotransmitter and neuroendocrine functions, is also involved in tumorigenesis. Results provide insight into molecular basis of serotonin in pancreatic cancer.

2016-05-12 | GSE81355 | GEO

Expression Profile of Embryonic Stem Cell Derived Serotonin Neurons

2009-05-21 | GSE16168 | GEO

Cancer anorexia: the role of serotonin in hypothalamic resistance of the neuropeptide Y system [A358_GEO_hypocells]

Project description:Anorexia is a common symptom among cancer patients and contributes to malnutrition and insufficient food intake. In cancer-induced anorexia, food intake regulation in the hypothalamus appears to be impaired. A negative energy balance persists and accelerates muscle wasting and malnutrition. Moreover, it strongly affects mortality and survival in these patients. Here, we show that the neuropeptide Y system (NPY) appears to fail to respond adequately to changes in energy balance during cancer cachexia. In addition, we investigate the connection between serotonin and NPY release in hypothalamic cell lines. Hypothalamic neuronal cells mHypoE-46 (serotonin sensitive cells) and mHypoA-2/12 (serotonin unresponsive cells) were used to study the effect of serotonin on messenger NPY expression and NPY excretion.

2014-10-31 | E-GEOD-57189 | biostudies-arrayexpress

The serotonin neurotransmitter modulates virulence of enteric pathogens

Project description:RNA seq experiment was perfomed in the presence and absence of 10µM serotonin

2020-05-08 | GSE144795 | GEO

The effects of serotonin by Tph1 on skeletal muscle

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

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