This study aimed to explore the expression level of miR-539 in the blood-brain barrier permeability induced by cerebrovascular occlusion and its mediated mechanism. Altogether, 48 patients with cerebral vascular occlusion lesions from March 2018 to June 2020 were collected. The expression level of miR-539 in the peripheral blood serum of the subjects was analyzed by qRT-PCR, and the participants were divided into two groups according to the results of head and neck ultrasound and CTA hemodynamics. The MCAO model of cerebral ischemia was established in rats, and the expression level of miR-539 was detected by qRT-PCR in brain tissues of different groups of rats. The effects of miR-539 on the permeability of blood-brain barrier were investigated by intraventricular injection of agomiR-539 and antagomir-539. The model of blood-brain barrier was established by culturing brain microvascular endothelial cells and pericytes in vitro, and the changes of miR-539 expression level and permeability after glucose and oxygen deprivation were detected. The expression level of SNAI2/MMP9 signaling pathway protein in cells was detected by Western blot. Compared with the healthy control group, the expression level of miR-539 in peripheral blood of patients with cerebrovascular occlusive disease decreased significantly, and the expression level of miR-539 in the MCAO rat model decreased and affected the permeability of blood-brain barrier. Glucose and oxygen deprivation treatment in brain microvascular endothelial cells can lead to downregulation of miR-539 expression and affect cell permeability. miR-539 in brain microvascular endothelial cells can target and bind to SNAI2 and participate in the regulation of endothelial cell permeability by affecting the SNAI2/MMP9 signaling pathway. The results of this study suggested that circulating miR-539 in peripheral blood may be a potential marker for predicting blood-brain barrier permeability after ischemic stroke. More detailed studies are needed to determine its diagnostic value.

Voltage-gated Ca2+ channels play a key role in the regulation of arterial tone and blood pressure. The aim of this study was to determine whether the association of calcium voltage-gated channel subunit alpha1 C (CACNA1C) rs1006737 with essential hypertension (EH) exists in both Chinese Han and ethnic Russian populations of Northeast Asia. We used a case-control study of 2 ethnic groups in the same latitude geographical area to investigate the association between the susceptibility of EH and rs1006737 polymorphism. A total of 1512 EH patients and 1690 controls in Chinese Han people (Heilongjiang Provence, China), 250 EH patients, and 250 controls in ethnic Russian people (Chita, Russia), participated in this study. All participants were genotyped using the TaqMan SNP genotyping assay (Agena Company). Baseline characteristics and the minor allele frequencies of rs1006737 vary substantially among common Chinese Han and ethnic Russian people. Allele A was found to be a risk factor for EH in Chinese Han [(odds ratio) OR 1.705, (confidence interval) 95% CI: 1.332–2.182, P < .001] and ethnic Russian (OR 1.437; 95% CI: 1.110–1.860, P = .006). The GA genotype was significantly associated with an increased risk of hypertension (OR 1.538, 95% CI: 1.188–1.991, P = .001) for Chinese Han people, and the AA genotype (OR 2.412, 95% CI: 1.348–4.318, P = .003) for ethnic Russian people. The results of this study indicate that the A allele of the variant rs1006737 in the CACNA1C gene may be a useful genetic marker for EH risk prediction in Chinese Han and ethnic Russian populations.