Release date: 2016-04-18
Blood flows through the blood vessels, transporting oxygen and nutrients throughout the body, and the process has a complex set of reactions that are regulated by cell-specific gene expression. In a recent study published in the international academic journal Nature Communication, Yale researchers found that a key mediator can participate in the intracellular reaction process, and also demonstrated how the factor affects the formation of new blood vessels.
GPCR signals play an important role in the development of blood vessels, including apelin (APLN) and its receptor APLNR. However, this is still not revealing how the ligand-receptor regulates a series of downstream signaling pathways.
In this study, the researchers used mouse and zebrafish models to find a small RNA molecule, microRNA139-5p, that directly affects the dialogue between two GPRC signaling pathways that determine neovascular growth. The necessary cellular response. They further revealed how blood flow affected this dialogue.
The researchers found that deletion of Apln, Aplnr or endothelial cell-specific deletion of Aplnr caused severe retinal vascular disorders in mice, and increased expression of endothelial cell CXCR4 played a part. It was found that endothelial cell CXCR4 is negatively regulated by miR-139-5p, and both blood laminar flow and APLN/APLNR signaling can induce transcription of miR-139-5p.
Inhibition of miR-139-5p under in vivo conditions can partially mimic the retinal vascular defect phenotype caused by APLN/APLNR deletion. Inhibition of CXCR4 signaling by drugs or enhancement of the miR-139-5p-CXCR4 signal axis can attenuate defects caused by APLN/APLNR deletion.
The author of the article, Dr. Hyung J. Chun, said that they have a deeper understanding of the process of vascular development. These findings have implications for the treatment of cancers involved in the process of neovascularization and the treatment of diseases such as heart disease.
Source: Bio Valley
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