Transcriptomic profiling of the telomerase transformed Mesenchymal stromal cells derived adipocytes in response to rosiglitazone.
Adipogenesis
Brown adipocytes
Differentiation
Rosiglitazone
Telomerase-transformed mesenchymal stromal cells (iMSC3)
Transcriptomic analysis
White adipocytes
mRNA-seq
Journal
BMC genomic data
ISSN: 2730-6844
Titre abrégé: BMC Genom Data
Pays: England
ID NLM: 101775394
Informations de publication
Date de publication:
09 03 2022
09 03 2022
Historique:
received:
18
08
2021
accepted:
17
01
2022
entrez:
10
3
2022
pubmed:
11
3
2022
medline:
3
5
2022
Statut:
epublish
Résumé
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. 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. Rosiglitazone regulated several differentially regulated genes and non-coding RNAs that warrant further investigation about their roles in adipogenesis particularly brown adipogenesis.
Sections du résumé
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 further investigation about their roles in adipogenesis particularly brown adipogenesis.
Identifiants
pubmed: 35264099
doi: 10.1186/s12863-022-01027-z
pii: 10.1186/s12863-022-01027-z
pmc: PMC8905835
doi:
Substances chimiques
Rosiglitazone
05V02F2KDG
Telomerase
EC 2.7.7.49
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17Informations de copyright
© 2022. The Author(s).
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