Transcriptomic profiling of the telomerase transformed Mesenchymal stromal cells derived adipocytes in response to rosiglitazone
Al-Ali MM., Khan AA., Fayyad AM., Abdallah SH., Khattak MNK.
Laboratory Study, published in BMC Genom Data (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
- BMC Genom Data (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35264099
- PMCID
- PMC8905835
- DOI
- 10.1186/s12863-022-01027-z
- Citations
- 6
Abstract (original English)
Background Differentiation of Immortalized Human Bone Marrow Mesenchymal Stromal Cells - hTERT (iMSC3) into adipocytes is in vitro model of obesity. In our earlier study, rosiglitazone enhanced adipogenesis particularly the brown adipogenesis of iMSC3. In this study, the transcriptomic profiles of iMSC3 derived adipocytes with and without rosiglitazone were analyzed through mRNA sequencing. Results A total of 1508 genes were differentially expressed between iMSC3 and the derived adipocytes without rosiglitazone treatment. GO and KEGG enrichment analyses revealed that rosiglitazone regulates PPAR and PI3K-Akt pathways. The constant rosiglitazone treatment enhanced the expression of Fatty Acid Binding Protein 4 (FABP4) which enriched GO terms such as fatty acid binding, lipid droplet, as well as white and brown fat cell differentiation. Moreover, the constant treatment upregulated several lipid droplets (LDs) associated proteins such as PLIN1. Rosiglitazone also activated the receptor complex PTK2B that has essential roles in beige adipocytes thermogenic program. Several uniquely expressed novel regulators of brown adipogenesis were also expressed in adipocytes derived with rosiglitazone: PRDM16, ZBTB16, HOXA4, and KLF15 in addition to other uniquely expressed genes. Conclusions Rosiglitazone regulated several differentially regulated genes and non-coding RNAs that warrant furthe
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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