Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Age-associated adipose-derived stem cell activity is dictated by IGF2BP3-dependent regulation of glutamine and BCAA catabolism

ABSTRACT: Age-associated adipose-derived stem cell activity is dictated by IGF2BP3-dependent regulation of glutamine and BCAA catabolism

PROVIDER: PRJNA1112872 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29099804_1.fastq.gz	Fastqsanger.gz
	SRR29099804_2.fastq.gz	Fastqsanger.gz
	SRR29069952_1.fastq.gz	Fastqsanger.gz
	SRR29069952_2.fastq.gz	Fastqsanger.gz
	SRR29069953_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

Age-associated adipose-derived stem cell activity is dictated by IGF2BP3-dependent regulation of glutamine and BCAA catabolism

Project description:Aging-related diseases were commonly considered being attribute to age-dependent loss in numbers or differentiation potential, whereas aging effects on stem cell characteristics were poorly concerned. In the present study, we investigated age-related alterations of human adipose-derived stem cells (hASCs) from infant (I-hASCs) and elderly (E-hASCs) donors. Based on the integration of multi-omics analyses including scRNA-seq, proteomic, and metabolomic profiles, we unveiled the ACTA2+TAGLN+ cluster primarily confers hASC stemness and tissue repair function. In particular, E-hASCs exhibited attenuated BCAA and glutamine catabolism, potentially due to the decreased BCAT1 and GLS expression in ACTA2+TAGLN+ cluster, which subsequently reduced the energy production and ROS elimination ability of hASCs. Mechanistic studies revealed that BCAT1 and GLS were positively regulated by IGF2BP3 which was diminished in the ACTA2+TAGLN+ cluster of E-hASCs. Suppression of IGF2BP3 decreased I-hASCs self-renewal and multidirectional differentiation potential through the negative regulation of redox homeostasis and energy production, whereas BCAT1 or GLS expression can partly reverse the negative effect of IGF2BP3 knockdown. Furthermore, m6A modification of BCAT1 or GLS mRNAs is required for IGF2BP3-mediated mRNA stability, as demonstrated by the use of METTL3 shRNA or m6A inhibitors. Glutamine and BCAA supplementation effectively restored E-hASC self-renewal and multidirectional differentiation potential both in vitro and in vivo, suggesting the clinical application value to E-hASCs therapy in the treatment of aging-related diseases or in the wound healing for elder.

2024-04-29 | PXD051832 |

Age-associated adipose-derived stem cell activity is dictated by IGF2BP3-dependent regulation of glutamine and BCAA catabolism

Project description:Cultured human adipose-derived stem cells(hASCs) are considered as a homogeneous population in vitro. We used single cell RNA sequencing (scRNA-seq) to reveal the cellular heterogeneity of hASCs and identify aging-related cell clusters in hASCs.

2025-05-20 | GSE267783 | GEO

BCAA catabolic mutants in prolonged darkness

Project description:We used RNA-Seq to ask whether the transcripts for the proposed BCKDH subunits are upregulated in wild-type plants subjected to prolonged darkness. These experiments were performed using rosette leaves from 5-week-old, short-day-grown (8h light/16h dark) Col-0 wild-type plants moved to constant darkness for 6h, 24h, 48h and 72h, and grown in short day for 72h as control. The transcripts of eight BCAA catabolism genes were increased nine- to 400-fold within the first 6h of prolonged darkness, and remained high until the last time point. These results are consistent with the hypothesis that BCAA catabolic enzymes - including BCKDH subunits E1A1, E1B1, E1B2 and E2 - have one or more physiological roles in the dark. Rosette leaf mRNA profiles of 5-week old Col wild type (WT, CS60000) and BCAA catabolic mutants ivd1-2 and hml1-2 were generated byRNA sequencing, in duplicate, using Illumina HiSeq2500.

2015-04-16 | E-GEOD-67956 | biostudies-arrayexpress

Heme Biosynthesis Regulates BCAA Catabolism and Thermogenesis in Brown Adipose Tissue

Project description:Heme Biosynthesis Regulates BCAA Catabolism and Thermogenesis in Brown Adipose Tissue

| PRJNA1222362 | ENA

Defective Branched-Chain Amino Acid Catabolism in Dorsal Root Ganglia Contributes to Mechanical Pain

Project description:Impaired branched-chain amino acid (BCAA) catabolism has recently been implicated in the development of mechanical pain, but the underlying molecular mechanisms are unclear. Here we report that defective BCAA catabolism in dorsal root ganglion (DRG) neurons sensitizes mice to mechanical pain by increasing lactate production and expression of the mechanotransduction channel Piezo2. In high-fat diet-fed obese mice, we observe downregulation of PP2Cm, a key regulator of the BCAA catabolic pathway, in DRG neurons. Mice with conditional knockout of PP2Cm in DRG neurons exhibit mechanical allodynia under normal or SNI-induced neuropathic injury conditions. Furthermore, the VAS scores in the plasma of patients with peripheral neuropathic pain are positively correlated with BCAA contents. Mechanistically, defective BCAA catabolism in DRG neurons promotes lactate production through glycolysis, which increases H3K18la modification and drives Piezo2 expression. Inhibition of lactate production or Piezo2 silencing attenuates the pain phenotype of knockout mice in response to mechanical stimuli. Therefore, our study demonstrates a causal role of defective BCAA catabolism in mechanical pain by enhancing metabolite-mediated epigenetic regulation.

2023-08-27 | GSE235230 | GEO

PROX1 Orchestrates Tumor Metabolic Plasticity by Integrating LKB1-AMPK Signaling with BCAA Catabolism

Project description:PROX1 Orchestrates Tumor Metabolic Plasticity by Integrating LKB1-AMPK Signaling with BCAA Catabolism

| PRJNA884334 | ENA

BCAA catabolic mutants in prolonged darkness

2015-04-16 | GSE67956 | GEO

Heme Biosynthesis Regulates BCAA Catabolism and Thermogenesis in Brown Adipose Tissue

Project description:The distinctive color of brown adipose tissue (BAT) is attributed to its high content of heme-rich mitochondria. Despite this, the mechanisms by which BAT regulates intracellular heme levels remain largely unexplored. Here, we demonstrate that heme biosynthesis is the primary source of heme in brown adipocytes. Inhibiting heme biosynthesis results in an accumulation of the branched-chain amino acids (BCAAs) valine and isoleucine, due to a heme-associated metabolon that channels BCAA-derived carbons into heme biosynthesis. Heme synthesis-deficient brown adipocytes display reduced mitochondrial respiration and lower UCP1 levels compared to wild-type cells. While exogenous heme supplementation can restore intracellular heme levels and mitochondrial function, UCP1 downregulation persists. This sustained UCP1 suppression is linked to epigenetic regulation induced by the accumulation of propionyl-CoA, a byproduct of disrupted heme synthesis. Finally, disruption of heme biosynthesis in BAT impairs thermogenic response and, in female, but not male, mice, hinders the cold- induced clearance of circulating BCAAs in a sex-hormone-dependent manner. These findings establish adipose heme biosynthesis as a key regulator of thermogenesis and sex-dependent BCAA homeostasis.

2025-02-18 | GSE289295 | GEO

IGF2BP3 controls cancer cell invasiveness by modulation RISC function

Project description:The goal of this study was to determine IGF2BP3 regulation of RNA targets in human pacreatic ductal adenocarcinoma cell lines Included are iCLIP-seq libraries for IGF2BP3 from PL45 and Panc1 PDAC cell samples, RIP-seq samples from PL45 and Panc1 PDAC cells, RNA-seq data sets from control and IGF2BP3 knockdown in PL45 and Panc1 PDAC cells, and small RNA-seq samples from Panc1 cells

2016-03-12 | E-GEOD-79147 | biostudies-arrayexpress

PROX1 Orchestrates Tumor Metabolic Plasticity by Integrating LKB1-AMPK Signaling with BCAA Catabolism (ATAC-Seq)

Project description:PROX1 Orchestrates Tumor Metabolic Plasticity by Integrating LKB1-AMPK Signaling with BCAA Catabolism (ATAC-Seq)

| PRJNA884343 | ENA