Platelet‐derived microparticles promote endothelial cell proliferation in hypertension via miR‐142–3p

Abstract

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.

Small extracellular vesicles from rat plasma promote migration and proliferation of vascular smooth muscle cells

“…3, 4). Other studies examined the effects of EV on cultured cells at wide-ranging concentrations between 10 5 -10 9 particles/ml [5,12,50]. Then, there was no obvious deviation in the concentrations of sEV used between ours and others'.…”

The Contrasting Role of Extracellular Vesicles in Vascular Inflammation and Tissue Repair

“…; which they detected as the most highly expressed microRNA in platelets, could be transferred to EC via platelet-derived EVs but not by platelets themselves (Bao et al, 2017). miR-142-3p suppressed the expression of target gene BCL2L1 and BCL2-associated transcription factor (BCLAF1) (Bao et al, 2017;Bao et al, 2018), resulting in increased proliferation and EC apoptosis in an in vivo rat model of hypertension. Upregulated EC proliferation and apoptosis play crucial roles in vascular remodeling associated with hypertension (Bao et al, 2017;Bao et al, 2018).…”

“…miR-142-3p suppressed the expression of target gene BCL2L1 and BCL2-associated transcription factor (BCLAF1) (Bao et al, 2017;Bao et al, 2018), resulting in increased proliferation and EC apoptosis in an in vivo rat model of hypertension. Upregulated EC proliferation and apoptosis play crucial roles in vascular remodeling associated with hypertension (Bao et al, 2017;Bao et al, 2018). In the same vein, the addition of stimulated platelet-derived miR-223 via EVs, resulted in a reduction of insulin-like growth factor-1 receptor with subsequent promotion of HUVEC apoptosis, triggered by advanced glycation end products (Pan et al, 2014).…”

The role of microvesicles containing microRNAs in vascular endothelial dysfunction

“…In hypertensive conditions, PMVs delivered miR‐142‐3p into ECs and then enhanced abnormal proliferation of ECs by acting on Bcl‐2‐associated transcription factor 1 (BCLAF1). These results indicate that PMVs transmit miR‐142‐3p from activated platelets into ECs and that miR‐142‐3p may play a crucial role in EC dysfunction . Anti‐β2‐glycoprotein I (anti‐β2GPI) antibodies are the most common antiphospholipid antibodies in antiphospholipid syndrome (APS).…”

“…These results indicate that PMVs transmit miR-142-3p from activated platelets into ECs and that miR-142-3p may play a crucial role in EC dysfunction. 88 Anti-β2-glycoprotein I (anti-β2GPI) antibodies are the most common antiphospholipid antibodies in antiphospholipid syndrome (APS).…”