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Platelet Microparticle-Derived MiR-320b Inhibits Hypertension with Atherosclerosis Development by Targeting ETFA
Yongcong He1, Yangyang Jiang2, Fan Wu1
1Department of Cardiology, Guangdong Second Provincial General Hospital.
Abstract:
Hypertension and atherosclerosis often occur simultaneously. This study aimed to explore the role and mechanism of platelet microparticle (PMP) -derived microRNA-320b (miR-320b) in patients with hypertension accompanied by atherosclerosis.We collected samples from 13 controls without hypertension and atherosclerosis and 20 patients who had hypertension accompanied by atherosclerosis. In vitro, platelets were activated by Thrombin receptor-activating peptide to produce PMPs. HUVECs were induced by CoCl2 to mimic a hypoxic environment in vitro. RT-qPCR was employed to detect the expression levels of CD61, miR-320b, and ETFA. The protein expression level of ETFA was evaluated via Western blotting. Furthermore, 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide, 5-ethynyl-2'-deoxyuridine, and wound healing assays were employed to assess the proliferation and migration of HUVECs. Enzyme-linked immunosorbent assay was used to measure the oxidative stress and inflammation-related factor expression.The expression of miR-320b was reduced in both platelets and PMPs but increased in plasma. MiR-320b promoted CoCl2-induced HUVEC viability, proliferation, and migration. The levels of the oxidative stress factors SOD and GSH as well as the inflammatory factor IL-10 were elevated in the CoCl2 + miR-320b mimics group compared with both the CoCl2 + mimics NC and CoCl2 groups. Conversely, the levels of the oxidative stress factors MDA and ROS as well as the inflammatory factors IL-6, TNF-α, and IL-1β were decreased. These results were regulated by miR-320b targeting ETFA.PMP-derived miR-320b inhibits the development of hypertension accompanied by atherosclerosis by targeting ETFA.
Insights
Platelet microparticle-derived microRNA-320b (miR-320b) plays a protective role in hypertension and atherosclerosis. Lower miR-320b levels in patients contribute to disease progression by targeting ETFA.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Hypertension and atherosclerosis frequently coexist, presenting a complex clinical challenge.
- Platelet microparticles (PMPs) are increasingly recognized as key mediators in cardiovascular disease.
- The specific role of microRNA-320b (miR-320b) derived from PMPs in this dual pathology remains unclear.
Purpose of the Study:
- To investigate the mechanism of PMP-derived miR-320b in patients with co-occurring hypertension and atherosclerosis.
- To elucidate the regulatory role of miR-320b in endothelial cell function under hypoxic conditions.
Main Methods:
- Sample collection from control subjects and patients with hypertension and atherosclerosis.
- In vitro induction of PMPs and hypoxic human umbilical vein endothelial cells (HUVECs).
- Quantitative real-time PCR (RT-qPCR), Western blotting, and various cell-based assays (MTT, EdU, wound healing) to assess gene/protein expression, cell viability, proliferation, migration, oxidative stress, and inflammation.
Main Results:
- miR-320b expression was decreased in platelets and PMPs but elevated in plasma of affected patients.
- miR-320b enhanced HUVEC viability, proliferation, and migration under hypoxic conditions.
- miR-320b modulated oxidative stress and inflammatory markers, with beneficial effects observed when miR-320b levels were increased.
- These effects were mediated by miR-320b targeting the ETFA gene.
Conclusions:
- PMP-derived miR-320b acts as a protective factor against the development of hypertension complicated by atherosclerosis.
- The inhibitory effect of miR-320b on disease progression is achieved through its regulation of ETFA and subsequent modulation of endothelial cell function, oxidative stress, and inflammation.
