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端粒酶转化的间充质基质细胞来源的脂肪细胞对罗格列酮反应的转录组谱分析。

Transcriptomic profiling of the telomerase transformed Mesenchymal stromal cells derived adipocytes in response to rosiglitazone.

机构信息

Department of Applied Biology, College of Sciences, University of Sharjah, Sharjah, 27272, UAE.

Human Genetics & Stem Cells Research Group, Research Institute of Sciences & Engineering, University of Sharjah, Sharjah, 27272, UAE.

出版信息

BMC Genom Data. 2022 Mar 9;23(1):17. doi: 10.1186/s12863-022-01027-z.

DOI:10.1186/s12863-022-01027-z
PMID:35264099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8905835/
Abstract

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.

摘要

背景

永生化人骨髓间充质基质细胞 - hTERT（iMSC3）向脂肪细胞分化是肥胖的体外模型。在我们之前的研究中，罗格列酮增强了脂肪生成，特别是 iMSC3 的棕色脂肪生成。在这项研究中，通过 mRNA 测序分析了有和没有罗格列酮的 iMSC3 衍生脂肪细胞的转录组谱。

结果

在没有罗格列酮处理的情况下，iMSC3 和衍生的脂肪细胞之间有 1508 个基因表达差异。GO 和 KEGG 富集分析表明，罗格列酮调节 PPAR 和 PI3K-Akt 通路。持续的罗格列酮处理增强了脂肪酸结合蛋白 4（FABP4）的表达，其富集了 GO 术语，如脂肪酸结合、脂滴以及白色和棕色脂肪细胞分化。此外，持续处理上调了几个与脂滴（LDs）相关的蛋白，如 PLIN1。罗格列酮还激活了受体复合物 PTK2B，该复合物在米色脂肪细胞的产热程序中具有重要作用。在有罗格列酮的情况下分化的脂肪细胞中还表达了几个独特表达的棕色脂肪生成新调控因子：PRDM16、ZBTB16、HOXA4 和 KLF15 以及其他独特表达的基因。

结论

罗格列酮调节了几个差异表达的基因和非编码 RNA，这些基因和非编码 RNA 需要进一步研究它们在脂肪生成，特别是棕色脂肪生成中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/ed0b839699fe/12863_2022_1027_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/44f9291f32fb/12863_2022_1027_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/71b46f5dcba6/12863_2022_1027_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/4d31675ba66a/12863_2022_1027_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/a13aee5f6e01/12863_2022_1027_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/04ea6fed0412/12863_2022_1027_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/31d5274c5f45/12863_2022_1027_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/41274cd25317/12863_2022_1027_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/5458196758ce/12863_2022_1027_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/ed0b839699fe/12863_2022_1027_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/44f9291f32fb/12863_2022_1027_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/71b46f5dcba6/12863_2022_1027_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/4d31675ba66a/12863_2022_1027_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/a13aee5f6e01/12863_2022_1027_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/04ea6fed0412/12863_2022_1027_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/31d5274c5f45/12863_2022_1027_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/41274cd25317/12863_2022_1027_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/5458196758ce/12863_2022_1027_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb1/8905835/ed0b839699fe/12863_2022_1027_Fig9_HTML.jpg

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