Platelet microRNAs and vascular injury
Elena V. Dolmatova, Kathy K. Griendling
Elena V. Dolmatova, Kathy K. Griendling
Published February 18, 2019
Citation Information: J Clin Invest. 2019;129(3):962-964. https://doi.org/10.1172/JCI127580.
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Commentary

Platelet microRNAs and vascular injury

Abstract

Vascular smooth muscle cell (VSMC) phenotype switching from a contractile state to a synthetic phenotype has been implicated in intimal remodeling during vascular injury. While multiple studies have focused on dedifferentiation of VSMCs, prevention of VSMC-mediated excessive repair remains poorly understood. In this issue of the JCI, Zeng et al. identified a mechanism by which platelet-derived microRNA-223 (miRNA-223) reverses VSMC dedifferentiation. The authors show that suppression of proliferation occurs after platelet internalization by VSMCs. Moreover, they demonstrate that miRNA-223 inhibits dedifferentiation and intimal hyperplasia in diabetic mice by decreasing PDGFRβ expression in VSMCs. Together, these results identify platelet-derived miRNA-223 as a potential therapeutic target in vascular injury.

Authors

Elena V. Dolmatova, Kathy K. Griendling

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Figure 1

Summary of the possible mechanisms for platelet-derived miRNA transfer during vascular injury.

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Summary of the possible mechanisms for platelet-derived miRNA transfer d...
With intact endothelium, platelets are quiescent. When the endothelial barrier is compromised, platelets are activated, form a clot, and release various factors promoting vessel repair. They also release microparticles (MPs) containing miRNAs that are taken up by endothelial cells (and possibly other cells) and exhibit various effects on protein expression in recipient cells. Next, the platelets are taken up by VSMCs and lysed, releasing miRNAs into cytoplasm of VSMCs. In particular, miRNA-223, -143, and -145 released in VSMC cytoplasm decrease expression of PDGFRβ, KLF5, and KLF4, thereby suppressing VSMC dedifferentiation and excessive repair.