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Next Generation Sequencing Analysis of primary rat lung fibroblast transcriptomes

ABSTRACT: Next Generation Sequencing Analysis of primary rat lung fibroblast transcriptomes

PROVIDER: PRJNA821442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18533854.fastq.gz	Fastqsanger.gz
	SRR18533855.fastq.gz	Fastqsanger.gz
	SRR18533856.fastq.gz	Fastqsanger.gz
	SRR18533857.fastq.gz	Fastqsanger.gz
	SRR18533858.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Analysis of primary rat lung fibroblast transcriptomes

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Next generation sequencing analysis of primary rat lung fibroblast, primary rat lung alveolar type 2 cell and a novel 10-4A rat lung cell line transcriptomes

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Next Generation Sequencing Analysis of Wild Type Mouse Embryonic Fibroblast (MEFs) Transcriptomes Stimulated by Viral Mimics

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Next Generation Sequencing Facilitates Quantitative Analysis Of Wild Type And Tbk1 N129D KI Murine Embryonic Fibroblast Transcriptomes

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Genome wide analysis of gene expression of rat ES cells, rat embryonic fibroblast cells and mouse ES cells

Project description:Rat ES cells were derived using 3I medium from E4.5 blastocysts. Rat embryonic fibroblast cells were derived form E14.5 embryos. To analyze the mechanism under the selfrenewal of rat ES cells, microarrays were used for the genome wide analysis of gene expressoin profiles in rat ES cells. Rat embryonic fibroblast cells and mouse ES cells were tested at same time as control. Our results from clustering analysis demonstrated that the gene expression profile of rat ES cells resembles mouse ES cells, but not REFs. Keyword: 3I medium; rat embryonic stem cells; mouse ES cells; rat embryonic fibroblast cells

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Next Generation Sequencing of Wild Type and CMG2-/- Rat Lung Transcriptomes

Project description:Purpose:Pulmonary arterial hypertension secondary to congenital heart disease (CHD-PAH) with systemic-to-pulmonary shunt is characterized by proliferative vascular remodeling. Capillary morphogenesis gene-2 (CMG2) exhibits roles in cell proliferation and apoptosis. The purpose of this study was to determine the possible roles of CMG2 in the pathogenesis of systemic-to-pulmonary shunt induced PAH. Methods Lung tissue sections from CHD-PAH patients, systemic-to-pulmonary shunt induced PAH rat model, CMG2-/- rats, and PASMCs were used. Immunohistochemistry, real time polymerase chain reaction, Western blot, proliferation, apoptosis, and next generation sequencing (NGS) were performed in this study. Results CMG2 expression was reduced in lung tissues and pulmonary arterioles from Eisenmenger’s syndrome patient and rats with systemic-to-pulmonary shunt induced PAH. CMG2-/- rats exhibited heavier PAH and pulmonary vascular remodeling following exposure to systemic-to-pulmonary shunt for 8 weeks. Over-expression of CMG2 in cultured human PASMCs inhibited cell proliferation and promoted apoptosis, while knockdown of CMG2 promoted cell proliferation and inhibited apoptosis. A total of 1319 genes were found to be dysregulated in CMG2-/- rat lungs as detected by NGS. Biological processes influenced by these differentially expressed genes include regulation of blood vessel diameter, vasoconstriction, regulation of blood vessel size, vascular process in circulatory system, etc., and the most prominent pathway regulated is PI3K-Akt signaling pathway. Conclusion Our work identifies a novel role for CMG2 in systemic-to-pulmonary shunt induced PAH based on the findings that CMG2 deficiency could exacerbate systemic-to- pulmonary shunt induced vascular remodeling in the development of PAH. CMG2 may be a potential target for CHD-PAH treatment.

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