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Inflammatory vascular disease: miRNAs in blood vessel damage miRNA molecules that inhibit the activity of specific genes are implicated in a cellular control network involved in some of the damaging effects of inflammation on blood vessels. Researchers in South Korea led by Young-Myeong Kim at Kangwon National University School of Medicine, Chuncheon, identified the link by studying cells from patients with the inflammatory condition pre-eclampsia, characterized by hypertension. They found that two miRNAs, miR-31 and miR-155, are involved in molecular signaling processes that impair the production of endothelial progenitor cells lining blood vessels, which is essential for maintenance and repair. The research also identified the key protein eNOS involved in the miRNA molecules’ mechanism of action. Understanding these miRNAs and the protein involved in their production and action may help researchers develop new treatments for blood vessel diseases associated with inflammation.

Vascular disease: Small RNA as a possible culprit The overexpression of a microRNA molecule adversely affects the functioning of vascular smooth muscle cells (VSMCs) and may contribute to the development of artherosclerosis and preeclampsia. The interactions between VSMCs and the cells lining blood vessels (endothelium) are crucial for maintaining the healthy phenotype and relaxation of blood vessels. Disruption to these interactions via inflammation, for example, can trigger serious vascular diseases. Young-Myeong Kim at Kangwon National University, Chungcheon, South Korea, and co-workers demonstrated that expression levels of a microRNA-155 are elevated in patients with artherosclerosis and preeclampsia, while an enzyme found in VSMCs called soluble guanylyl cyclase is considerably reduced. Using human and mice tissues, the team showed that miR-155 impairs the contractile phenotype and relaxation of VSMCs by reducing guanylyl cyclase expression. Their findings may inform new therapies for vascular diseases.