Hemodynamic effect of apelin in a canine model of acute pulmonary thromboembolism

Feng, Jinghui; Li, Weimin; Wu, Xiuping; Tan, Xiang-Yang; Gao, Yanhui; Han, Chong; Li, Shuqing; Xie, Huaning

doi:10.1016/j.peptides.2010.06.004

Cited by 17 publications

(14 citation statements)

References 29 publications

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“…Although vasodilator effects have been reported for apelin in the systemic circulation 11 , we found no evidence that Aplnr knockout affects vasoreactivity of the pulmonary circulation. Similar to our data, others have shown that administration of apelin to normal anesthesized dogs has no effect on the mean pulmonary artery pressure 18 . Fourth, we demonstrate that absence of Erg expression in venous endothelium confers proliferative capacity on PVECs, and that restoration of either Erg or Aplnr expression attenuates proliferation of venous endothelial cells in vitro .…”

Section: Discussionsupporting

confidence: 92%

ERG-APLNR Axis Controls Pulmonary Venule Endothelial Proliferation in Pulmonary Veno-Occlusive Disease

et al. 2014

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Background Pulmonary veno-occlusive disease (PVOD) is caused by excessive cell proliferation and fibrosis which obliterates the lumen of pulmonary venules, leading to pulmonary hypertension, right ventricular failure, and death. This condition has no effective treatment and a 5-year survival of less than 5%. Understanding the mechanism of this disease and designing effective therapies is urgently needed. Methods and Results We show that mice with homozygous deletion of the Ets transcription factor, Erg, die between E16.5 and three months of age from PVOD, capillary hemorrhage, and pancytopenia. We demonstrate that Erg binds to and serves as a transcriptional activator of the G-protein-coupled receptor gene, Aplnr, whose expression in the vasculature is uniquely specific for venous endothelium, and that knockout of either Erg or Aplnr results in pulmonary venous-specific endothelial proliferation in vitro. We show that mice with either homozygous-global or endothelial-directed deletion of Aplnr manifest PVOD and right heart failure, detectable at 8 months of age. Levels of pulmonary ERG and APLNR in patients with PVOD undergoing lung transplantation were significantly lower than those of controls. Conclusions Our results suggest that ERG and APLNR are essential for endothelial homeostasis in venules in the lung and that perturbation in ERG-APLNR signaling is crucial for the development of PVOD. We identify this pathway as a potential therapeutic target for the treatment of this incurable disease.

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Section: Discussionsupporting

confidence: 92%

ERG-APLNR Axis Controls Pulmonary Venule Endothelial Proliferation in Pulmonary Veno-Occlusive Disease

et al. 2014

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“…It is also known that the highest apelin mRNA expression is in the pulmonary tissue [4]. The effect of apelin on vasomotor tone is variable and may have different effects on the arterial vascular pressure in different pathophysiological conditions [15]. Apelin creates an antagonistic effect on vasoconstrictors by inhibiting reactive oxygen species and increasing NO synthesis [16,17].…”

Section: Discussionmentioning

confidence: 99%

Diagnostic value of serum apelin-13 in patients with pulmonary thromboembolism

Karataş¹

2018

Ann Clin Anal Med

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Aim: We aimed to investigate whether serum apelin-13 value could be a novel biomarker in the diagnosis of pulmonary thromboembolism (PTE). Material and Method: The study included 142 patients, 82 of which were diagnosed with PTE and 60 were control cases. Serum apelin-13 level was measured using venous blood samples with the ELISA kit. Results: The serum apelin level was 2219.4 ± 65.2 ng/mL in the PTE group and 1234.7 ± 35.5 ng/mL in the control group (p<0.05). Serum apelin-13 was 2495.8 ± 738.0 ng/mL in the DVT (+) group and 2118.0 ± 496.8 ng/mL in the DVT (-) group (p=0.009). The best cutoff value for apelin-13 in the control and PTE groups was determined as 1579 ng/mL. Sensitivity was 92.7% and specificity was 96.7% (95% confidence interval: 0.939 to 0.995, area under ROC curve: 0.979, p<0.001). Discussion: This study showed that serum apelin-13 value can be used as new diagnostic biomarker in patients with PTE. Apelin-13 value also elevates in patients with DVT (+). These results suggest that apelin-13 value may be used as a novel biomarker in the patients with acute PTE and DVT (+) in future practice.

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“…To date, only animal studies have examined apelin's involvement in acute PE. 10 In an acute PE, apelin may possess either protective vasodilator or vasoconstrictor effects within the pulmonary vessels. 11 This study aimed to investigate the possible involvement of the endogenous apelin within the pathophysiological events in patients with PE.…”

Section: Introductionmentioning

confidence: 99%