Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hypoxia induced cholecystokinin gene expression in 3D engineered muscle.

ABSTRACT: At high altitude, hypoxic atmosphere decreases the oxygen partial pressure (pO2) in the body, inducing several metabolic changes in tissues and cells. Furthermore, it exerts potent anorectic effects, thus causing energy deficit. Two decades ago, a marked increase in the level of resting plasma cholecystokinin (CCK) was observed at Mt. Kanchenjunga basecamp (BC) located at 5,100 m above the sea level, compared to sea-level control values. Interestingly, acute exercise also raises plasma CCK and exerts potent anorectic effects under normoxic conditions. However, the molecular mechanism underlying these effects has not yet been established. We employed acute electrical pulse stimulation (EPS), followed by a microarray analysis, to discover novel myokines in 3D engineered muscle. Acute EPS efficiently affects the contractile function, inducing a decline of the contractile force. Surprisingly, microarray analysis revealed an EPS-induced activation of the cholecystokinin receptor (CCKR)-mediated signaling. Furthermore, Cck was constitutively expressed in 3D engineered muscle, and was upregulated by hypoxic conditions. Notably, a hypoxia responsive element (HRE) was detected in the Cck promoter of mice and humans. Our results suggested that, under hypoxic conditions, Hif-1a binding to HRE transactivated Cck expression in mice and humans. Furthermore, the plasma CCK elevation after acute exercise or at high altitude might be partly attributed to myogenic cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE135373 | GEO | 2021/04/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Peripheral blood mononuclear cell (PBMC) gene expression in healthy adults rapidly transported to high altitude

Project description:Differential expression analysis comparing healthy volunteers at sea level and after acute exposure to altitude

2013-04-30 | GSE46480 | GEO

Comparison of gene expression in whole blood of mice subjected to normobaric hypoxia in vivo.

Project description:To determine hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic hypoxic environment, equivalent to an altitude of 6500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic, normobaric conditions by exposing them to ambient air in Philadelphia (c. 50 mts above sea level).

2010-04-25 | GSE15894 | GEO

Peripheral blood mononuclear cell (PBMC) gene expression in healthy adults rapidly transported to high altitude

Project description:Differential expression analysis comparing healthy volunteers at sea level and after acute exposure to altitude PBMCs were isolated from healthy volunteers participating in the United States Antarctic Program. Array data was processed using the Affymetrix HG U133 Plus 2 array

2013-04-30 | E-GEOD-46480 | biostudies-arrayexpress

Immunoglobulin-like domain receptor 1 mediates fat-stimulated cholecystokinin secretion.

Project description:Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells of the small intestine. CCK is released into blood following a meal; however, the mechanisms inducing hormone secretion are largely unknown. Ingested fat is the major stimulant of CCK secretion. We recently identified a novel member of the lipoprotein remnant receptor family known as immunoglobulin-like domain containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the signal for fat-stimulated CCK secretion. In the intestine, ILDR1 is expressed exclusively in CCK cells. Orogastric administration of fatty acids elevated blood levels of CCK in wild type but not ILDR1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained. The uptake of fluorescently labeled lipoproteins in ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique combination of fatty acid plus HDL. CCK secretion secondary to ILDR1 activation is associated with increased [Ca2+]i consistent with regulated hormone release. These findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids and lipoproteins and that absorbed fatty acids regulate gastrointestinal hormone secretion. GFP positive cells from CCK-EGFP transgenic mice were isolated by FACS and the expression profile was compared with an equal number of non-fluorescent intestinal cells.

2013-05-23 | E-GEOD-47196 | biostudies-arrayexpress

Gene expression profiling under exposure to high altitude hypoxic environment

Project description:Understanding molecular mechanism associated with high altitude exposure during acclimatization/adaptation/maladaptation. Data reveals specific components of the complex molecular circuitry underlying high altitude pulmonary edema. Individualized outcome prediction were constructed through expression profiling of 39400 genes in sea level sojourners who were acclimatized to high altitude and grouped as controls (n=14), high altitude natives (n=14) and individuals who developed high altitude pulmonary edema within 48-72 hours after air induction to high altitude (n=17).

2013-12-18 | E-GEOD-52209 | biostudies-arrayexpress

Gene expression of Mus exposed to chronic hypoxia

2009-04-30 | GSE15891 | GEO

Plasma proteomics analysis of individuals at high altitude and sea level revealed by LC-MS/MS

Project description:We aim to investigate the changes of plasma proteome between sea level and high altitude, between AMS patients and non-AMS controls.

2023-09-21 | PXD045131 | iProX

Immunoglobulin-like domain receptor 1 mediates fat-stimulated cholecystokinin secretion.

2013-05-23 | GSE47196 | GEO

Transcription profiling of mouse exposed to chronic hypoxia

Project description:High altitude environments are characterized by the unique and unavoidable stress of chronic hypoxia. While much is known about gene expression responses to acute or in vitro hypoxia, less is known about the gene expression profiles of animals exposed to systemic chronic hypoxia, such as that experienced at high elevations. Here we simulated the hypoxic environment of two high altitude elevations,and a third chamber recieved ambient Reno air. Mice were housed in the hypoxic chambers for 32 days. We used microarrays to characterize the differential gene expression in the livers of mice housed in hypoxic environment of 4500 m versus 3000 and 1400 m. We used this data to draw hypotheses related to novel physiological responses to chronic systemic hypoxia Experiment Overall Design: Mice were housed one of three chambers; the first received ambient Reno air (1400 m) and the other two received air mixed with nitrogen such that one chamber simulated the hypoxic environment of 3000 m and the third chamber simulated hypoxic environment of 4500 m. Twelve mice were housed in each chamber for 32 days. Liver were extracted, and RNA from livers of 4 mice were pooled such that each treatment was represented by 3 pooled samples. Eight of the nine arrays were used for data analysis; one array was excluded as several Affymetrix quality control metrics indicated data quality that was not reliable.

2009-05-11 | E-GEOD-15891 | biostudies-arrayexpress

Effect of CCK-8s injection (20 ug/kg BW i.p.) on mRNA translational activity in hypothalamic oxytocin neurons of mice fed standard chow or high-fat/high-sugar diet (RiboTag;TRAP)

Project description:Oxytocin-expressing paraventricular hypothalamic neurons (PVN^OT neurons) integrate afferent signals from the gut including cholecystokinin (CCK) to adjust whole-body energy homeostasis. However, the molecular underpinnings by which PVN^OT neurons orchestrate gut-to-brain feeding control remain unclear. Here, we show that mice undergoing selective ablation of PVNOT neurons fail to reduce food intake in response to CCK and develop hyperphagic obesity on chow diet. Notably, exposing wildtype mice to a high-fat/high-sugar (HFHS) diet recapitulates this insensitivity towards CCK, which is linked to diet-induced transcriptional and electrophysiological aberrations specifically in PVNOT neurons. Restoring OT pathways in DIO mice via chemogenetics or polypharmacology sufficiently re-establishes CCK?s anorexigenic effects. Lastly, by single-cell profiling, we identify a specialized PVN^OT neuronal subpopulation with increased ?-opioid signaling under HFHS diet, which restrains their CCK-evoked activation. In sum, we here document a novel (patho)mechanism by which PVN^OT signaling uncouples a gut-brain satiation pathway under obesogenic conditions.

2023-09-07 | GSE242245 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data