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RNA-seq of female mouse cerebral cortex with vehicle or 17-beta estradiol treatment

ABSTRACT: RNA-seq of female mouse cerebral cortex with vehicle or 17-beta estradiol treatment

PROVIDER: PRJEB6753 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR566365.fastq.gz	Fastqsanger.gz
	ERR566366.fastq.gz	Fastqsanger.gz
	ERR566367.fastq.gz	Fastqsanger.gz
	ERR566368.fastq.gz	Fastqsanger.gz
	ERR566369.fastq.gz	Fastqsanger.gz

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RNA-seq of female mouse cerebral cortex with vehicle or 17-beta estradiol treatment

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Mechanism of 17-β Estradiol Stimulated Integration of Human Mesenchymal Stem Cells in Heart Tissue

Project description:Scarcity of gender specific donor hearts highlights the importance of mesenchymal stem cells (MSCs) as a therapeutic tool for heart repair. However, inefficient incorporation, retention, and activity of MSCs in cardiac tissue remains an obstacle. Since surge in follicular estradiol (μmolar-range) triggers tissue remodeling (e.g. ovulation) and estradiol exerts beneficial actions on the cardiovascular system, we hypothesized that estradiol may promote/improve MSC-mediated cardiac repair processes. Methods: Wharton’s jelly-derived MSCs were used, to assess the effects of estradiol on their proliferation, directed-migration and engraftment in murine heart slices, ex vivo. Results: MSCs expressed estrogen receptors (ERs) α and β, and estradiol promoted MSC proliferation (measured using xCELLigence real-time cell-impedance system and DNA-quantification). Estradiol up-regulated mRNA (qRT-PCR) and protein expression (western blotting) of ERα, ERβ, EMMPRIN, and MMP-9, yet down-regulated MMP-2 expression. In MSCs estradiol, up-regulated mRNA expression of VEGF-A, VCAM-1, and angiogenin, and stimulated NO production via ER. Proteomic analysis revealed that in MSCs estradiol up-regulated 47 proteins, down-regulated 7 proteins, and increased the expression of key biochemical components/pathways involved in tissue repair. In MSCs co-cultured with murine heart-slices, estradiol significantly induced MSC migration in an ER-dependent fashion (and preferentially via ERα) and significantly increased the secretion of MMP-2, MMP-9, angiogenin and VEGF. Conclusion: Estradiol facilitates the integration/engraftment of MSCs into heart slices by promoting MSC proliferation and migration and these beneficial effects are mediated via increases in molecules/pathways involved in tissue remodeling and angiogenesis. Priming of MSCs with estradiol may enhance their ability to repair/regenerate cardiac tissue in women.

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