Endothelial cells (ECs) are located at the interface between flowing blood and the vessel wall, and abnormal EC proliferation induced by pathologic environments plays an important role in vascular remodeling in hypertensive conditions. Exchanges of information between blood components and ECs are important for EC function. Hence, the present study sought to determine how platelets induce EC dysfunction under hypertensive conditions. EC proliferation was increased in renal hypertensive rats established by abdominal aortic coarctation compared with control rats and that elevated thrombin in plasma promoted platelet activation, which may induce the release of platelet-derived microparticles (PMPs). MicroRNA (MiR) array and qPCR revealed a higher level of miR-142-3p in platelets and PMPs. In vitro, PMPs delivered miR-142-3p into ECs and enhanced their proliferation via Bcl-2-associated transcription factor (BCLAF)1 and its downstream genes. These results indicate that PMPs deliver miR-142-3p from activated platelets into ECs and that miR-142-3p may play important roles in EC dysfunction in hypertensive conditions and may be a novel therapeutic target for maintaining EC homeostasis in hypertension.-Bao, H., Chen, Y.-X., Huang, K., Zhuang, F., Bao, M., Han, Y., Chen, X.-H., Shi, Q., Yao, Q.-P., Qi, Y.-X. Platelet-derived microparticles promote endothelial cell proliferation in hypertension via miR-142-3p.

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We propose a homogeneous circular polarizer based on a bilayered chiral metamaterial with two enantiomeric wheel patterns. The transmitted field of an arbitrarily polarized incident wave through this bilayered structure is nearly circularly polarized with a circular polarization extinction ratio of more than 30 dB at resonance. We show that the origin of this phenomenon is the excitation of spinning electric dipoles in the wheel patterns, which blocks the transmission of one-handed circularly polarized component but exert little influence on the other. We also demonstrate that the operation bandwidth can be enhanced by stacking functional layers in the propagation direction.

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Emerging evidence implicates elevated activity of STAT3 transcription factor in driving the development and progression of diabetic cardiomyopathy (DCM). We hypothesized that the fibrosis-promoting and hypertrophic actions of STAT3 are linked to the activation by epidermal growth factor receptor (EGFR). We tested this hypothesis by challenging cultured cardiomyocytes to high-concentration glucose and heart tissues of streptozotocin (STZ)-induced type 1 diabetic mice. Our results indicated that, in diabetic mice, the blockade of STAT3 or EGFR using selective inhibitors S3I-201 and erlotinib, respectively, abrogated the increased activating STAT3 phosphorylation and the induction of genes regulating fibrosis and hypertrophy in myocardial tissue. S3I-201 and erlotinib significantly reduced myocardial structural and functional deficits in diabetic mice. In cultured cardiomyocytes, high-concentration glucose induced EGFR-mediated STAT3 phosphorylation. We further showed that blockade of STAT3 or EGFR using selective inhibitors and siRNAs significantly reduced the increased expression of genes known to promote fibrosis and hypertrophy in cardiomyocytes. These results provide novel evidence that the EGFR-STAT3 signaling axis likely plays a crucial role in the development and progression of DCM.