Bony Breathlessness

Cockbain, Beatrice Clare; Price, Laura; Hind, Matthew

doi:10.1161/circulationaha.119.040833

Cited by 1 publication

(2 citation statements)

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“…Pulmonary arterial hypertension (PAH) is a disease typically characterized by pulmonary artery contraction, progressive pulmonary vascular resistance increase, and pulmonary artery pressure rise, which can lead to fatal right heart failure [1][2][3][4]. Pulmonary arterioles are composed of endothelial cells, smooth muscle cells, and fibroblasts [5][6][7]; among which, pulmonary smooth muscle cells are the main…”

Section: Discussionmentioning

confidence: 99%

“…Under the current circumstances, it is of great significance to uncover the mechanism of PAH under hypoxia to improve the prognosis, survival rate, and quality of life of patients with pulmonary heart disease induced by chronic hypoxia pulmonary diseases [ 3 , 4 ]. Some studies suggested that a variety of growth factors can be produced in the lung during hypoxic conditions to stimulate the proliferation of smooth muscle cells, elastic fibers, and collagen fibers in the inner membrane, resulting in pulmonary vascular remodeling [ 5 , 6 ]. PAH caused by such vascular remodeling may be relevant to a number of mechanisms such as phenotypic changes of pulmonary smooth muscle cells [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-146-5p Promotes Pulmonary Artery Endothelial Cell Proliferation under Hypoxic Conditions through Regulating USP3

Zhang

2021

Disease Markers

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Objective. MicroRNAs play a pivotal role in the progression of pulmonary hypertension (PAH). Although microRNA-146-5p is specifically expressed in many diseases, but in PAH, its role remains elusive. Patients and Methods. 30 patients with PAH and 20 healthy volunteers in our hospital were enrolled, and their serum samples were extracted for the detection of microRNA-146-5p and ubiquitin specific protease 3 (USP3) expression. In addition, the interaction between microRNA-146-5p and USP3 was examined by luciferase reporting assay. Furthermore, the potential mechanism was explored by cell counting kit-8 (CCK-8), 5-ethynyl-2 ′ -deoxyuridine (EdU), and Western blotting experiments. Results. It was found that microRNA-146-5p was higher in PAH patients than in healthy volunteers. Meanwhile, in hypoxia-induced human pulmonary artery endothelial cell lines (HPAECs), microRNA-146-5p expression was dramatically downregulated while USP3 protein expression was conversely upregulated. Under hypoxic conditions, microRNA-146-5p mimics was able to prompt the growth of HPAECs. In addition, after overexpression of microRNA-146-5p, luciferase reporting assay revealed a reduced luciferase activity of the reporter gene containing the USP3 3 ′ -untranslated region, and a reduction of USP3 protein expression was also confirmed. However, USP3 overexpression partially attenuated the impact of upregulated microRNA-146-5p on the proliferation capacity of HPAECs. Conclusions. MicroRNA-146-5p was able to enhance the proliferation ability of HPAEC cells under hypoxic conditions through targeting USP3, suggesting the microRNA-146-5p/USP3 axis may act as a target for PAH treatment.

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