Vitamin A-Derived Retinoic Acid Contributes to Muscle Stem Cell and Mitochondrial Function [scRNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1117907 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29224842_1.fastq.gz | Fastqsanger.gz | |||
| SRR29224842_2.fastq.gz | Fastqsanger.gz | |||
| SRR29224843_1.fastq.gz | Fastqsanger.gz | |||
| SRR29224843_2.fastq.gz | Fastqsanger.gz |
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Project description:Vitamin A is an exogenous micronutrient that is derived solely from diet and metabolized into retinoic acid, which acts as an antioxidant and transcriptional regulator. Here we show that obstruction of dietary Vitamin A drives mitochondrial and cell cycle dysfunction in MuSCs and myoblasts that mimics old age. The receptor for vitamin A derived retinol, Stra6, was found to be diminished with MuSC activation and in old age. The loss of Stra6 in myogenic progenitors resulted in accumulation of mitochondrial reactive oxygen species, as well as changes in mitochondrial morphology and respiration. Pharmacological targeting of Stra6 and retinoic acid signaling in myogenic progenitors and aged MuSCs reverted oxidative damage, enhanced mitochondrial function, and improved maintenance of quiescence. These results demonstrate that Vitamin A regulates mitochondria and metabolism in MuSCs to promote quiescence. These results highlight a unique mechanism connecting stem cell function with vitamin intake.
2024-06-03 | GSE268617 | GEO
Project description:Vitamin A is an exogenous micronutrient that is derived solely from diet and metabolized into retinoic acid, which acts as an antioxidant and transcriptional regulator. Here we show that obstruction of dietary Vitamin A drives mitochondrial and cell cycle dysfunction in MuSCs and myoblasts that mimics old age. The receptor for vitamin A derived retinol, Stra6, was found to be diminished with MuSC activation and in old age. The loss of Stra6 in myogenic progenitors resulted in accumulation of mitochondrial reactive oxygen species, as well as changes in mitochondrial morphology and respiration. Pharmacological targeting of Stra6 and retinoic acid signaling in myogenic progenitors and aged MuSCs reverted oxidative damage, enhanced mitochondrial function, and improved maintenance of quiescence. These results demonstrate that Vitamin A regulates mitochondria and metabolism in MuSCs to promote quiescence. These results highlight a unique mechanism connecting stem cell function with vitamin intake.
2024-06-03 | GSE268616 | GEO
Project description:Vitamin A-Derived Retinoic Acid Contributes to Muscle Stem Cell and Mitochondrial Function [RNA-Seq]
| PRJNA1117908 | ENA
Project description:Observational studies in human suggest involvement of vitamin A/retinoic acid (RA) signaling in the regulation of airway smooth muscle (ASM) function, but the precise mechanisms by which RA impacts ASM phenotype is not clear. Here, we generated trascriptional profiles from primary human ASM from 3 unrelated donoros cultured in control medium or medium containing BMS493 (an retinoic acid receptor antagonist)
2018-12-25 | GSE116845 | GEO
Project description:Observational studies in human suggest involvement of vitamin A/retinoic acid (RA) signaling in the regulation of airway smooth muscle (ASM) function, but the precise mechanisms by which RA impacts ASM phenotype is not clear. Here, we generated trascriptional profiles from two different models of RA-sufficient and RA-deficient mouse ASM in order to determine the molecular targets of RA in ASM (VAS/VAD, CTR/BMS) Mouse ASMs were isolated from Acta2-hrGFP;Cspg4-DsRED adult mice using flow cytometry. VAS mice were given normal, vitamin A-sufficient diet (15 IU vitamin/g) while the VAD mice were given 3 days of vitamin A-deficient diet (< 0.1 IU vitamin/g). CTR/BMS mouse ASMs were also isolated from Acta2-hrGFP;Cspg4-DsRED adult mice using flow cytometry. CTR mice were given 3 days of powdered, vitamin A sufficient diet mixed with vehicles (corn oil) while the BMS diet were given 3 days of powdered, vitamin A sufficient diet mixed with a potent pan-RA-receptor antagonist (BMS, 5 mcg/g).
2018-12-25 | GSE116846 | GEO
Project description:Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improving dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate and supplemented), and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P<0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding RARß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log26 in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naïve rats. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling RBP4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change. All rats were housed in a room maintained at 22°C with a 12-h dark:light cycle, and food and water were freely available. For the Steady-State Vitamin A Study (experiment 1) and the Retinoic Acid 16-hour Kinetic Study (experiment 2), lactating female Sprague-Dawley rats with 12 female pups (purchased from Charles River Laboratories, Willmington, MA) were fed a vitamin A-deficient purified diet [AIN-93G diet, prepared by Research Diets, New Brunswick, NJ] to reduce the transfer of vitamin A in milk from mother to pups prior to the start of the study. For experiment 1, from weaning, the offspring were fed the same diet modified to contain vitamin A at one of four levels: 0 (vitamin A deficient), 0.4 mg retinol/kg diet (vitamin A marginal), 4 mg retinol/kg diet (vitamin A adequate control), or 100 mg retinol/kg diet (vitamin A supplemented). All rats were studied at 8 weeks of age. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. In experiment 2, at 8 weeks of age female vitamin A-deficient rats were treated with ~100 ug of All-trans-Retinoic acid (at-RA) for 0 (vehicle only), 3, 6, 10 or 16 h (n=3-4/group). Tissues were collected and RNA was prepared in the same manner as in experiment 1. In the 90-minute "first pass" kinetic study (experiment 3), female rats were purchased at 6 weeks of age and fed a stock rodent diet. When the rats were 8 weeks old they were assigned to a control (naïve) group. Rats in the naive group received an equal amount of vehicle only (vegetable oil/5% ethanol). Food was removed immediately. Sixteen hours after priming, each rat was lightly anesthetized by isoflurane-oxygen inhalation and treated with ~25 ug all-trans-RA bound to albumin [10 ug RA per 100 g bo dy weight], injected into the exposed left common iliac vein. The incision was closed with a surgical staple. The rats were allowed to recover from the anesthesia. Rats were killed at 0 minute (vehicle injection), and 30, 60, and 90 min (n = 3/group) after injection of the RA test dose. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. For experiment 1, five biological repeats were Vitamin A deficient, seven biological repeats were Vitamin A marginal, six biological repeats were Vitamin A adequate, and two biological repeats were Vitamin A supplemented. In experiment 2, three biological repeats were performed for each of the following treatments: untreated, at-RA for 3 hours, at-RA for 6 hours and at-RA for 16 hours. Four biological repeats were treated with at-RA for 10 hours. For experiment 3, two biological repeats were untreated and three biological repeats were performed for each of the following at-RA treatment times: 30, 60 and 90 minutes. A total of 47 samples were analyzed.
2011-08-31 | E-GEOD-24104 | biostudies-arrayexpress
Project description:Exit from HSC dormancy is controlled via vitamin A/retinoic acid
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Project description:Using H9C2 cardiomyoblasts, we have shown that all-trans retinoic acid (ATRA), the biologically active metabolite of vitamin A, affects mitochondrial dynamics at 10nM concentration. The low dose ATRA stimulates the expression of nuclear retinoid receptors and induces mechanisms that are protective against severe point damage caused by laser irradiation at the mitochondrial level. To determine the protective effect of ATRA against photodamage, we used the proteomic analysis based on liquid chromatography and mass spectrometry (LC-MS/MS) to compare the abundancies of proteins between control and ATRA-treated cardiomyoblasts.
2022-02-23 | PXD026967 | Pride
Project description:The maintenance of skeletal muscle tissue is of pivotal importance in health and disease, as its loss is often associated with chronic or progressive pathologies, generally worsening the prognosis. Increased levels of vitamin D binding protein (VDBP) in biological samples were reported to co-occur with several pathologies susceptible to muscle wasting, including various types of tumors. We, therefore, hypothesized that VDBP may participate in muscle wasting and investigated its direct effects on skeletal muscle homeostasis. Here we demonstrate that VDBP induces atrophy independently of vitamin D. In C2C12 myotubes, we identified the perturbation of the intracellular actin dynamic and subsequent mitochondrial dysfunction as the main molecular mechanisms at the basis of VDBP-induced atrophy. Coherently, the ectopic introduction of VDBP in mice lacking the protein (Gc-knockout mice; Gc-KO) induces muscle atrophy, the dismantling of neuromuscular junctions, and decreased force. Finally, we provide proof-of-concept evidence that VDBP contributes to cancer-associated muscle wasting. Altogether, these findings provide novel insights into the biological function of VDBP and have potential implications for the treatment of muscle wasting.
2026-02-20 | PXD042024 | Pride
Project description:mRNA expression of hearts obtained from mice with Stimulated by retinoic acid gene 6 (Stra6) germline deletion, Vitamin A deficiency (VAD) induced by lecithin-retinol acyltransferase (Lrat) germline deletion and feeding with vitamin A-deficient diet, and the combination of both. Mice were subjected to myocardial infarction (MI) or Sham surgery.
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