Itaconic Acid as A Differential Transcription Regulator of Apoptosis and Autophagy Pathways Genes: A Rat Adipose Mesenchymal Stem Cells Model.
Tabandeh MR., Soroush F., Dayer D.
Laboratory Study on Chronic Inflammation, published in Cell J (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Cell J (2022)
- Country
- Iran
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 36259476
- PMCID
- PMC9617019
- DOI
- 10.22074/cellj.2022.8320
- Citations
- 1
Abstract (original English)
Objective Itaconate, a novel regulatory immunometabolite, is synthesized by inflammatory macrophage. It acts as an anti-inflammatory mediator and regulates several metabolic and signaling pathways particularly Nrf2 pathway. The immunometabolites can affect the stemness potency, differentiation ability and viability of stem cells, but little is known about the critical function of Itaconate on the stem cell fate. The objective of the present study was to determine the regulatory effects of Itaconic acid on the cell viability and transcription of apoptosis and autophagy pathways genes in the rat adipose derived mesenchymal stem cells (ADMSCs). Materials and methods In this experimental study, the ADMSCs were incubated with 125 μM and 250 μM dimethyl itaconate (DMI) for 24 hours or 48 hours. The expression of apoptosis pathway genes ( Bax, Bcl2, Caspase 3, Fas, Fadd and Caspase 8 ) and autophagy pathway genes ( Atg12, Atg5, Beclin, Lc3b and P62 ) were determined using real time polymerase chain reaction (PCR) assay. Using the ELISA method, cellular level of phospho-NRF2 protein was measured. Results The results indicated that DMI increased the expression of NRF2 protein, altered the expression of some apoptosis genes ( Fadd, Bax and Bcl2 ), and changed the expression of some autophagy related genes ( Lc3b, Becline and P62 ) in ADMSCs. DMI had no obvious effect on the transcription
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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