Abstract
Objective: Low plasma level of high-density lipoprotein cholesterol (HDL-C) associated with poor outcomes in several cardiovascular diseases, including pulmonary arterial hypertension (PAH). Regulation of miR-638 have been proved to be associated with PAH. The aim of this study was to evaluate the expression of miR-638 after Xuezhikang (XZK) therapy in patients with low HDL-C. Methods: Plasma levels of miR-638 were quantified by real-time polymerase chain reactions in 20 patients with PAH and 30 healthy controls. A total of 40 subjects with low HDL-C were assigned to receive an XZK therapy for 6 months. The miR-638 expression profiles were detected in PAH patients, XZK-treated subjects and lovastatin treated pulmonary arterial smooth muscle cells (PA-SMCs). Results: The relative expression level of miR-638 in the plasma was lower in the PAH patients than that in the controls (p < 0.001). An increase of 11.2% from baseline in the HDL-C level was found after XZK therapy (p < 0.001). The relative expression of miR-638 was increased after XZK treatment (p < 0.01). The changes of miR-638 were inversely associated with baseline HDL-C levels. A significantly reduction in miR-638 expression were found in PDGF-BB-treated hPA-SMCs compared to the control cells, and the pre-treatment of the cells with lovastatin significantly re-gain the expression levels in miR-638. Conclusion: In patients with low HDL-C levels, XZK therapy raised the expression of miR-638, suggesting that the potential therapeutic effect of XZK in PAH patients with low serum HDL-C levels deserves further exploration.
Highlights
Pulmonary arterial hypertension (PAH) is a devastating and lethal cardio-pulmonary disease (Hoeper et al, 2016)
The mean highdensity lipoprotein cholesterol (HDL-C) level was 1.19 ± 0.13 mmol/L after XZK treatment, representing an increase of 11.2% from baseline (p < 0.001)
We described the low expression of miR-638 in patients with low HDL-C for the first time
Summary
Pulmonary arterial hypertension (PAH) is a devastating and lethal cardio-pulmonary disease (Hoeper et al, 2016). Epidemiologic studies have demonstrated that low plasma level of highdensity lipoprotein cholesterol (HDL-C) was associated with poor outcomes in pulmonary arterial hypertension (Rayner et al, 2010). Several miRNAs have been demonstrated to regulate lipid metabolism, including miR-122, miR-370, miR-335, miR-378/378* and miR33 (Rayner et al, 2010; Rayner et al, 2011a; Rayner et al, 2011b; Kim et al, 2017; Agbu and Carthew, 2021). Previous studies have demonstrated that MCT resulted in significant pulmonary vascular remodeling and down-regulation of miR-638; miR638 mimics inhibited pulmonary arterial smooth muscle cells (PA-SMCs) proliferation and percentage of PCNA-positive cells in vitro (Luque et al, 2018; Liu et al, 2020; Mirhadi et al, 2021). The roles of miR-638 in lipid metabolism and expression profiles in patients with PAH are unclear
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