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ABSTRACT: MMA

PROVIDER: PRJNA289933 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR2103280_1.fastq.gz	Fastqsanger.gz
	SRR2103280_2.fastq.gz	Fastqsanger.gz
	SRR2103290_1.fastq.gz	Fastqsanger.gz
	SRR2103290_2.fastq.gz	Fastqsanger.gz
	SRR2103360_1.fastq.gz	Fastqsanger.gz

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Methylmalonic acid induces metabolic abnormalities and exhaustion in CD8+ T cells to suppress anti-tumor immunity

Project description:Systemic levels of methylmalonic acid (MMA), a byproduct of propionate metabolism, increase with age and MMA promotes tumor progression via its direct effects in tumor cells. However, the role of MMA in modulating the tumor ecosystem remains to be investigated. The proliferation and function of CD8+ T cells, key anti-tumor immune cells, declines with age and in conditions of vitamin B12 deficiency, which are the two most well-established conditions that lead to increased systemic levels of MMA. Thus, we hypothesized that increased circulatory levels of MMA would lead to a suppression of CD8+ T cell immunity. Treatment of primary CD8+ T cells with MMA induced a dysfunctional phenotype characterized by robust immunosuppressive transcriptional reprogramming and marked increases in the expression of the exhaustion regulator, TOX. Accordingly, MMA treatment upregulated exhaustion markers in CD8+ T cells and decreased their effector functions, which drove the suppression of anti-tumor immunity in vitro and in vivo. Mechanistically, MMA-induced CD8+ T cell exhaustion was associated with a suppression of NADH-regenerating reactions in the TCA cycle and concomitant defects in mitochondrial function. Thus, MMA has immunomodulatory roles, thereby highlighting MMA as an important link between aging, immune dysfunction, and cancer.

2024-10-17 | GSE256487 | GEO

compare of microRNA expression between IA and MMA

Project description:To exploring the difference of microRNA expression between IA and MMA, we have employed microRNA array expression profiling as a discovery platform to identify genes between the IA and MMA. Futher functional analyses were performed based on the data.

2013-04-25 | GSE46336 | GEO

compare of microRNA expression between IA and MMA

2013-04-25 | E-GEOD-46336 | biostudies-arrayexpress

compare of mRNA expression between IA and MMA

Project description:To exploring the difference of mRNA expression between IA and MMA, we have employed mRNA array expression profiling as a discovery platform to identify genes between the IA and MMA. It's a compensate experiment after microRNA array, we paired the mRNA data with miRNA targets, finally, these data were used for the functional analysis. 2 IA and 2 MMA tissue were used for the microarray

2013-04-25 | E-GEOD-46337 | biostudies-arrayexpress

compare of mRNA expression between IA and MMA

2013-04-25 | GSE46337 | GEO

Hormesis underlies the adaptive response in methylmalonic acidemia (MMA)

Project description:Methylmalonic acidemia (MMA), an organic acidemia characterized by metabolic instability and multiorgan complications, is most frequently caused by mutations in methylmalonyl-CoA mutase (MUT). To define the metabolic adaptations in MMA, in the chronic and acute settings, we studied a mouse model generated by transgenic expression of Mut in the muscle. Mut-/-;TgINS-MCK-Mut mice accurately replicate the hepato-renal mitochondriopathy and growth failure seen in severely affected patients, and were used to characterize the response to fasting. The hepatic transcriptome in MMA mice was characterized by the chronic activation of stress-related pathways and responded abberrantly to fasting when compared to controls.

2019-08-01 | GSE118862 | GEO

MethylMalonic Acidemia (MMA) is predicted by lipocalin-2 (LCN2) and attenuated by antioxidant therapy.

Project description:Isolated methylmalonic acidemia (MMA) is a pleiotropic enzymatic defect of branched-chain amino acid oxidation most commonly caused by deficiency of methylmalonyl-CoA mutase (MUT). End stage renal disease (ESRD) is emerging as an inevitable disease-related complication, recalcitrant to conventional therapies and liver transplantation. To establish a viable model of MMA-associated renal disease, methylmalonyl-CoA mutase (Mut) was expressed in the liver of Mut -/- mice as a stable transgene under the control of an albumin (INS-Alb-Mut) promoter. Mut -/- ;TgINS-Alb-Mut mice were rescued from the neonatal lethality displayed by Mut -/- mice and manifested a decreased glomerular filtration rate (GFR), chronic tubulointerstital nephritis (CTIN) and prominent ultrastructural changes in the proximal tubular mitochondria, replicating precisely the renal manifestations seen in a large MMA patient cohort. To explore the pathophysiological changes that underlie the renal disease of MMA, we compared gene expression profiles of whole kidney mRNA samples between 4 female Mut +/+, Mut +/- and Mut -/- ;TgINS-Alb-Mut mice after they ingested a HP diet for 2 months. Females were used because more survived the dietary challenge, whereas the histology, ultrastructure and GFR effects were identical between sexes

2013-05-01 | E-GEOD-41044 | biostudies-arrayexpress

Targeting proximal tubule mitochondrial dysfunction attenuates the renal disease of methylmalonic acidemia

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Serum differential proteomic profiling of patients with isolated methylmalonic acidemia by iTRAQ

Project description:The serum for 3 MMA patients and 3 healthy subjects were used for LC-MS/MS.Quantitative proteomic profiling of serum of patients with isolated MMA by iTRAQ labeling.

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