Recently, the underlying mechanism of vascular calcification (VC) has been partially elucidated. However, it is still high incidence, and no effective treatment has been found. This study aims at figuring out the underlying mechanisms of microRNA‐708‐5p (miR‐708‐5p)/sodium‐phosphate transporter 1 (Pit‐1) axis in high phosphate (HP)‐induced VC of T/G HA‐VSMCs. Alizarin Red S staining was used to evaluate calcium salt deposition, and the activity of alkaline phosphatase (ALP) was determined by measuring the absorbance at 405 nm. RT‐qPCR and Western blot were performed to assess the levels of miR‐708‐5p and Pit‐1, the levels of ALP, Pit‐1, β‐catenin, glycogen synthesis kinase 3 β (GSK3β), and p‐GSK3β proteins, respectively. The interaction between miR‐708‐5p and Pit‐1 was validated by luciferase reporter assay. Our findings illustrated that miR‐708‐5p was downregulated and Pit‐1was upregulated in HP‐induced VC. MiR‐708‐5p mimics inhibited HP‐induced VC. Further experiments demonstrated that miR‐708‐5p targets Pit‐1. In addition, miR‐708‐5p inactivates the Wnt8b/β‐catenin pathway via targeting Pit‐1 to reduce HP‐induced VC. MiR‐708‐5p has a crucial effect on VC via targeting Pit‐1 and inhibiting Wnt8b/β‐catenin pathway, it may serve as a new target for VC treatment.
Coronary heart disease (CHD) is the leading cause of death from cardiovascular disease. This study investigated the expression and clinical significance of long noncoding RNA (lncRNA) autophagy promoting factor (APF) in peripheral blood of patients with acute myocardial infarction (AMI) caused by CHD. Patients with angina pectoris (AP) (n = 80) and AMI (n = 96) and other patients (n = 60) with precordial discomfort but no CHD were included. The serum levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, CDR1AS, miR-188-3 p, and cardiac troponin I (cTnI)/creatine kinase (CK)/creatine kinase isozymes (CK-MB) were detected using reverse transcription-quantitative polymerase chain reaction or enzyme-linked immunosorbent assay. Patients with AMI were divided into high/low expression groups based on the median level of APF, and the clinical baseline indicators of patients with AMI were compared. The correlation between lncRNA APF and cTnI/CK/ CK-MB/miR-188-3p was analyzed using Pearson analysis, and the clinical value of lncRNA APF was evaluated using the receiver operating characteristic curve. The levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, and CDR1AS in patients with AMI were increased, whereas there were no differences in patients with AP. The APF levels in patients with AMI were higher than MIAT, MALAT1, and CHAST, whereas there were no differences between APF and H19 and CDR1AS. In patients with AMI, the high level of lncRNA APF was correlated with the history of smoking/drinking. Moreover, lncRNA APF was positively correlated with cTnI/CK/ CK-MB levels and negatively correlated with miR-188-3p. LncRNA APF has high diagnostic efficacy for AMI. Overall, lncRNA APF is highly expressed in patients with AMI caused by CHD and has high diagnostic efficacy for AMI.
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