apelin-13-peptide and Pulmonary-Embolism

Expression and peptide immunoreactivity of apelin messenger RNA have been described in a variety of tissues, including gastrointestinal tract, adipose tissue, brain, kidney, liver, cardiovascular system, and lungs. This study aimed to investigate the possible involvement of the endogenous apelin in the pathophysiological events that occur in patients with pulmonary embolism (PE).. In total, 53 patients with PE and 35 healthy volunteers were included the study. This cross-sectional study was conducted at a tertiary care university hospital and among patients diagnosed as having PE. The control group consisted of healthy volunteers who applied to hospital for a routine checkup examination. Serum apelin 13 levels were measured in both the groups and their results were compared.. The median ages were 57 and 53 years, and female-male ratios were 30/23 and 20/15, in the PE and control groups, respectively. The mean serum apelin 13 levels were found to be significantly higher in the PE group (76.94 ± 10.70 ng/mL) than in the control group (50.01 ± 7.13 ng/mL; P < .001).. This study demonstrated that apelin 13 levels are elevated in patients with PE. These results suggest that apelin may be a novel biomarker and a potential therapeutic target in patients with acute PE in the future.

Topics: Biomarkers; Case-Control Studies; Cross-Sectional Studies; Female; Humans; Intercellular Signaling Peptides and Proteins; Male; Middle Aged; Pulmonary Embolism

The peptide apelin is expressed in the pulmonary vasculature and is involved in the pathogenesis of many cardiovascular diseases. It has a biphasic role in the regulation of vasomotor tone related to the vascular endothelium. In this study, we induced acute pulmonary embolism (APE) in dogs with autologous blood clots to assess the effect of apelin on pulmonary and systemic circulation in the acute phase of APE. The expression of apelin mRNA was found to be upregulated in the lung tissue in the early several hours after APE induction and decreased at 24 h. The expression of apelin protein in the pulmonary arteries did not change within 24 h after APE, but significantly increased in the bronchial epithelial cells as early as 1h and decreased at 24 h. In normal anesthetized dogs, intravenous bolus administration of apelin significantly reduced the mean arterial pressure (MAP), but did not significantly affect the mean pulmonary arterial pressure (MPAP). In the dogs with APE, apelin decreased MPAP, whereas its impact on MAP was not significantly different from that in the control group. Taken together, the level of endogenous apelin did not change significantly in the pulmonary arterial wall, whereas its expression in the bronchial epithelium was upregulated in the early stage of APE. The effect of exogenous apelin on vasomotor tone was complicated: it resulted in differential changes in the pulmonary and systemic arterial pressures under different physiological and pathological conditions.

Topics: Animals; Bronchi; Dogs; Epithelium; Female; Gene Expression Regulation; Hemodynamics; Intercellular Signaling Peptides and Proteins; Ligands; Lung; Male; Organ Specificity; Peptides; Pulmonary Circulation; Pulmonary Embolism; Random Allocation; Receptors, G-Protein-Coupled; RNA, Messenger; Time Factors