It has been reported that RhoA activation and Rho-kinase (ROCK) expression are increased in chronic hypoxic lungs, and the long-term inhibition of ROCK markedly improves the survival of patients with pulmonary arterial hypertension (PAH). However, whether Rho-kinase α (ROCK2) participates in regulation of the growth of pulmonary arterial endothelial cells (PAECs) remains unknown. The aim of the present study was to investigate the effect of hypoxia on the proliferation of PAECs and the role of ROCK2 in the underlying mechanism. The results of western blotting and reverse transcription-quantitative polymerase chain reaction analysis showed that hypoxia increased the activity and expression of ROCK2 in PAECs, and the stimulating effects of hypoxia on the proliferation of PAECs were attenuated by either the ROCK inhibitor Y27632 or transfection with ROCK2 small interfering RNA. Moreover, analysis of cyclin A and cyclin D1 mRNA expression indicated that ROCK2 mediates the cell cycle progression promoted by hypoxia. These results indicate that hypoxia promotes the proliferation of pulmonary arterial endothelial cells via activation of the ROCK2 signaling pathway.
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http://dx.doi.org/10.3892/etm.2016.3214 | DOI Listing |
Medicine (Baltimore)
January 2025
National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
The correlation between cathepsins and pulmonary arterial hypertension (PAH) is well-established, but the causative link between them remains uncertain. This study aimed to explore the causal role of circulating metabolites mediating cathepsins in PAH using Mendelian randomization (MR). A 2-sample 2-step MR method was used to identify causal relationship between cathepsins and PAH; causal relationship between circulating metabolites and PAH; and mediated effects of these circulating metabolites.
View Article and Find Full Text PDFInterdiscip Cardiovasc Thorac Surg
January 2025
Department of Pediatrics, Kansai Medical University, Hirakata, Osaka, Japan.
Objectives: This retrospective study aimed to investigate the feasibility of surgical closure of ventricular septal defect in children with trisomy 18 by assessing perioperative events and long-term survival.
Methods: From April 2008 to March 2024, 41 consecutive patients were referred to us for ventricular septal defect surgery. The defect was closed in 35 patients at the end (median age, 16 months; median body weight, 5.
Animal Model Exp Med
January 2025
Department of Pharmacology, Shantou University Medical College, Shantou, Guangdong, China.
Background: To investigate the toxicity of N-n-butyl haloperidol iodide (F2), a quaternary ammonium salt derivative of haloperidol, in mice for potential therapeutic purposes.
Methods: The acute median lethal dose (LD) of F2 was determined using the Bliss method following intravenous administration in mice. Routine surface electrocardiograms (ECGs) and arterial blood pressures (aBPs) were recorded under general anesthesia in untreated and pharmacologically vagotomized mice injected with F2.
Scand J Prim Health Care
January 2025
Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Aim: To investigate the association between Systematic Coronary Risk Evaluation 2 (SCORE2) and subclinical damage in two vascular beds: atherosclerosis in the coronary arteries and aortic arterial stiffness, in a large population-based cohort without cardiovascular disease or diabetes.
Methods: A cross-sectional study based on Swedish CArdio Pulmonary bioImaging Study (SCAPIS) data. A population-based cohort of 3087 participants aged 50-64.
J Cardiovasc Dev Dis
January 2025
Emergency Department, Leszek Giec Upper-Silesian Medical Centre of the Medical University of Silesia in Katowice, 40-635 Katowice, Poland.
Paradoxical embolism occurs when a clot originates in the venous system and traverses through a pulmonary or intracardiac shunt into the systemic circulation, with a mortality rate of around 18%. The risk factors for arterial embolism and venous thrombosis are similar, but different disease entities can lead to a hypercoagulable state of the blood, including antithrombin III (AT III) deficiency. We report the case of a 43-year-old man with a massive central pulmonary embolism with a rider embolus and concomitant aortic arch embolism with involvement of the brachiocephalic trunk, bilateral subclavian and axillary arteries, and the right vertebral artery, followed by a secondary ischaemic stroke.
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