MiR-410 inhibition induces HUVECs proliferation and represses ox-LDL-triggered apoptosis through activating STAT3.

Ox-LDL-induced endothelial cells injury has been reported to play an important role in the development of atherosclerosis (AS). MicroRNAs have been identified to regulate their target genes post-transcriptionally and they are able to participate in the various diseases, including AS. However, the role of miR-410 in ox-LDL-triggered abnormal function of endothelial cells remains to be elaborated. Hence, our current study was to find out the underlying mechanism of miR-410 in AS. Here, we observed that ox-LDL can inhibit HUVECs growth and lead to a great cell apoptosis both dose-dependently and time-dependently. Meanwhile, it was exhibited that miR-410 expression was remarkably elevated in ox-LDL-indicated HUVECs. miR-410 knockdown was able to induce cell proliferation and alleviate HUVECs apoptosis subjected to ox-LDL. Reversely, signal transducer and activator of transcription 3 (STAT3) expression was greatly decreased in ox-LDL-incubated HUVECs in a time and dose dependent manner. Additionally, these findings exhibited that STAT3 was a target of miR-410, which was validated by a dual-luciferase assay in our study. Additionally, we observed that overexpression of STAT3 rescued ox-LDL induced AS events in vitro. Taken these together, our current study implied that miR-410 silence can inhibit the ox-LDL-induced HUVECs proliferation and rescue cell apoptosis through activating STAT3 in vitro.

[Autoantibodies against alpha1 adrenergic receptor related with cardiac remodeling in hypertensive patients by clinical observation].

OBJECTIVE: To investigate the effects of autoantibodies against alpha(-) adrenergic receptor on cardiac remodeling in patients with hypertension. METHODS: Five hundred and fifty three patients with hypertension in our hospital were selected. The autoantibodies against alpha(1) adrenergic receptor in sera of donor were detected by ELISA, and the results of echocardiography were recorded. By multiple logistic regressions, the risk factors were analyzed on left ventricular enlargement of hypertension. RESULTS: The percentage of autoantibodies against alpha(1) adrenergic receptor positive was 32.3% (179/553). There were significant difference between the positive group and negative group on the ratio of left atrial enlargement (53.6%, 44.3%, respectively; P < 0.05) and left ventricular enlargement (12.8%, 6.1%, respectively; P < 0.01). The result of regression analysis demonstrated that 4 risk factors were related to left ventricular enlargement, including male, course of disease, heart rate (HR) and autoantibodies against alpha(1) adrenergic receptor in the serum (all P < 0.05). CONCLUSIONS: The autoantibodies against alpha(1) adrenergic receptor have a relationship with left ventricular enlargement of hypertension. Patients with the activity of autoantibodies against alpha(1) adrenergic might contribute to predict cardiac remodeling.