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A Time-series transcriptome analysis of Rosiglitazone effects in mice neonatal cardiomyocytes.

ABSTRACT: Rosiglitazone is a member of the thiazolidinedione class of drugs, an anti-diabetic drug known for being a ligand of peroxisome proliferation activating receptors γ (PPARγ), a group of nuclear hormone receptors that are involved in the regulation of genes related to glucose and lipid metabolism. The use of Rosiglitazone has been shown to increase the risk of congestive heart failure in type II diabetes patients due to increased fluid retention and plasma volume. Our data show that the effects of Rosiglitazone on cardiomyocytes occur really early within a great increase in magnitude in time but consistent in the pathways affected. Also, the initial deleterious effect triggers a protective molecular response at 24 hours of exposure that is maintained at 48h but also accompanied by further activation of the system that can damage the heart.

ORGANISM(S): Rattus norvegicus albus

PROVIDER: GSE117198 | GEO | 2020/02/26

REPOSITORIES: GEO

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Project description:Trophoblasts, as the main part of placenta, undergo cell differentiation including invasion, migration, and fusion. Abnormalities in these processes can lead to a series of gestational diseases whose underlying mechanisms are still unclear. The peroxisome proliferator-activated receptor γ (PPARγ), expressed in the nuclei of extravillous trophoblasts (EVCTs) at the first trimester and villous cytotrophoblasts (VCTs) throughout the pregnancy, is proved to be essential in placentation. We aimed to explore the genome-wide effects of PPARγ on EVCTs and VCTs by the treatment of PPARγ agonist rosiglitazone. EVCTs and CTs were purified from human chorionic villi, followed by primary culture and rosiglitazone treatment. Transcriptomes of EVCTs and VCTs were performed by microarray experiments (Affymetrix and Axon). Owing to the different platforms, threshold for differentially expressed genes (DEGs) detection was performed based on 1.5-fold change and 5% FDR for EVCTs gene expression while 1% FDR was set for VCTs gene expression. Gene ontology (GO) annotation and pathways analysis of DEGs were conducted with ClueGO. PPARγ and DEGs protein interactions predicted by online tool STRING, while PPARγ and DEGs promoters binding sites prediction was conducted by iRegulon. GO and pathway terms were compared between EVCTs and VCTs through ClusterProfiler. Visualization was achieved and modified by Cytoscape. Our microarray data showed that 139 DEGs were detected in rosiglitazone-treated EVCTs (RT-EVCTs) and 197 DEGs in rosiglitazone-treated VCTs (RT-VCTs). Downstream annotation analysis showed the commons and differences between RT-EVCTs and RT-VCTs, including biological process, molecular function, cellular component, KEGG pathway and protein-protein-interaction and transcription factor – target gene binding site prediction. To sum up, our results provide a sight of view to PPARγ-activated trophoblasts performances by giving transcriptomic signatures of the RT-EVCTs and RT-VCTs and make it feasible to acquire more information for further research and find out possible drug-targeted genes or pathways in human placenta.

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A Time-series transcriptome analysis of Rosiglitazone effects in mice neonatal cardiomyocytes.

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