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MiR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death

ABSTRACT: miR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death

PROVIDER: PRJNA862172 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20634830_1.fastq.gz	Fastqsanger.gz
	SRR20634830_2.fastq.gz	Fastqsanger.gz
	SRR20634832_1.fastq.gz	Fastqsanger.gz
	SRR20634832_2.fastq.gz	Fastqsanger.gz

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miR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death

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miR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death.

Project description:BackgroundBoth downregulation and elevation of microRNA miR-145 has been linked to an array of cardiopulmonary phenotypes, and a host of studies suggest that it is an important contributor in governing the differentiation of cardiac and vascular smooth muscle cell types.Methods and resultsTo better understand the role of elevated miR-145 in utero within the cardiopulmonary system, we utilized a transgene to overexpress miR-145 embryonically in mice and examined the consequences of this lineage-restricted enhanced expression. Overexpression of miR-145 has detrimental effects that manifest after birth as overexpressor mice are unable to survive beyond postnatal day 18. The miR-145 expressing mice exhibit respiratory distress and fail to thrive. Gross analysis revealed an enlarged right ventricle, and pulmonary dysplasia with vascular hypertrophy. Single cell sequencing of RNA derived from lungs of control and miR-145 transgenic mice demonstrated that miR-145 overexpression had global effects on the lung with an increase in immune cells and evidence of leukocyte extravasation associated with vascular inflammation.ConclusionsThese data provide novel findings that demonstrate a pathological role for miR-145 in the cardiopulmonary system that extends beyond its normal function in governing smooth muscle differentiation.

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Project description:Gallbladder carcinoma (GBC) is a rare cancer entity in Western Europe and the US with an incidence of less than 3/100.000 and a survival rate <10%. Radical surgery is the only potentially curative treatment option but most patients diagnosed with GBC are not resectable. Thus, there is a great need for the development of new treatment options, including targeted therapy for GBC. To dissect the epigenetic regulation during GBC development, we performed global miRNA profiling of 40 GBC and 8 normal gallbladder tissues. MiRNAs that are associated with survival were functionally analysed by cell proliferation and colony formation assays. In addition, we performed whole genome gene expression analysis of cells expressing miRNA mimics or control and performed biochemical assays to dissect miR-145 signalling. The GBC miRNA profiles exhibited large differences compared to normal gallbladder tissues with 49% of miRNAs being differentially expressed (FDR<0.001). In addition, 8 miRNAs were found to be down- and 16 to be up-regulated in the GBCs with poor outcome (p<0.05). The most down-regulated miRNA was miR-145-5p and the top up-regulated miRNA was miR-575. Overexpression of miR-145 led to a significant reduction of cell proliferation and colony formation, whereas opposite effects were observed for miR-575. Gene expression profiling of cells overexpressing miR-145 revealed activation of the STAT1 signalling pathway by inhibition of PTPRF in cholangiocellular but not hepatocellular carcinoma cells. Thereby, PTPRF directly bound to STAT1 and reduced STAT1 phosphorylation. This study identified pro- and anti-tumorigenic miRNAs in GBC and provides new mechanistic insight in the tumour suppressive function of miR-145 loss leading to active STAT1 signalling.

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