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The aim of the study was to investigate the expression of miR-155 in plasma and peripheral blood mononuclear cells (PBMCs), the effects of miR-155 on the apoptosis rate of PBMCs and the extent of coronary stenosis in coronary artery disease patients. Seventy chest pain patients were divided into three groups by symptoms, signs, auxiliary examination and coronary arteriography: 21 cases in the acute myocardial infarction group (AMI), 23 cases in the Angor pectoris group (AP) and 26 cases in the control group (CT). The peripheral blood mononuclear cells of the patients in the three groups were separated for cell culture. Annexin V/propidium iodide (PI) was performed to analyze cell apoptosis. RT-qPCR was used to evaluate the expression level of miR-155 in plasma and PBMCs. There were significant differences on the expression of miR-155 in plasma and PBMCs, the apoptosis rate of PBMCs, Gensini score and the extent of coronary stenosis among the three groups (P<0.05). The expression of miR-155 in plasma and PBMCs in AMI and AP group were lower than CT group while the AMI group was lower than the AP group (P<0.05). The apoptotic rate of PBMCs, Gensini score and the extent of coronary stenosis of the AMI and AP groups were higher than CT group while the AMI group was higher than the AP group (P<0.05). The expression of miR-155 in plasma was positively correlated with PBMCs, but negatively correlated with the apoptosis rate of PBMCs, Gensini score and the extent of coronary stenosis. The apoptosis rate of PBMCs in patients with coronary heart disease was positively correlated with the degree of coronary artery stenosis and Gensini score. In conclusion, in the patients with coronary heart disease the apoptosis rate of PBMCs was increased and the expression of miR-155 in plasma and PBMCs cells was decreased, which were correlated with the severity of coronary heart disease. [ABSTRACT FROM AUTHOR]

Focal adhesion kinase (FAK) is an important therapeutic target in pulmonary artery hypertension (PAH); however, the mechanism of its activation remains unknown. The present study aimed to investigate whether angiotensin-converting enzyme 2 (ACE2) could regulate FAK and alleviate PAH in a rat model of PAH established with a single administration of monocrotaline followed by continuous hypoxia treatment. In the current study, right ventricular pressure, body weight and the right ventricular hypertrophy index were measured, and hematoxylin-eosin staining was performed on lung tissues to determine whether the modeling was successful. Changes in the serum levels of FAK were measured using an ELISA kit to evaluate the association between ACE2 and FAK. The mRNA expression levels of ACE2, FAK, caspase-3 and survivin were determined using reverse transcription-quantitative PCR (RT-qPCR). The protein expression levels of ACE2, phosphorylated FAK/FAK, cleaved caspase-3/pro-caspase-3 and survivin were determined via western blotting. Immunohistochemistry was applied to detect the expression of FAK around the pulmonary arterioles. Apoptosis of smooth muscle cells around pulmonary arterioles was observed by TUNEL staining. After treatment with the ACE2 activator DIZE or inhibitor DX-600, the results demonstrated that ACE2 reduced PAH-induced changes in arteriole morphology compared with the control. It also inhibited FAK expression in serum. WB and RT-qPCR results suggested that ACE2 inhibited the expression of FAK and pathway-related proteins, and promoted caspase-3 expression. Additionally, ACE2 reduced FAK expression around the pulmonary arterioles and promoted smooth muscle cell apoptosis. The results indicated that ACE2 activation inhibited FAK expression, leading to alleviation of the symptoms of PAH. [ABSTRACT FROM AUTHOR]