ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
PAI-1 is a novel component of the miR-17~92 signaling that regulates pulmonary artery smooth muscle cell phenotypes.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- miR-17-5p: bridging the gap between disease mechanisms and therapeutic innovations.Epigenomics · 2025Review
- Cancer Cell-Derived Large Extracellular Vesicles Promote Venous Thromboembolism by Activating NETosis Through Delivering CYBA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Comprehensive insights and In silico analysis into the emerging role of LincRNAs in lung diseases pathogenesis; a step toward ncRNA precision.Functional & integrative genomics · 2025Review
- PAI-1 deficiency drives pulmonary vascular smooth muscle remodeling and pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Proteomics and Precise Exercise Phenotypes in Heart Failure With Preserved Ejection Fraction: A Pilot Study.Journal of the American Heart Association · 2023Article
- Adipokines in pulmonary hypertension: angels or demons?Heliyon · 2023Review
- Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- TMAO Upregulates Members of the miR-17/92 Cluster and Impacts Targets Associated with Atherosclerosis.International journal of molecular sciences · 2022Article
- Diagnostic value of miRNA expression and right ventricular echocardiographic functional parameters for chronic thromboembolic pulmonary hypertension with right ventricular dysfunction and injury.BMC pulmonary medicine · 2022Article
- Cellular mechanosignaling in pulmonary arterial hypertension.Biophysical reviews · 2021Review
- Non-Coding RNA Networks in Pulmonary Hypertension.Frontiers in genetics · 2021Review
- An Overview of miRNAs Involved in PASMC Phenotypic Switching in Pulmonary Hypertension.BioMed research international · 2021Review
- MicroRNA-137 Inhibited Hypoxia-Induced Proliferation of Pulmonary Artery Smooth Muscle Cells by Targeting Calpain-2.BioMed research international · 2021Article
- An Overview of the Cytoskeleton-Associated Role of PDLIM5.Frontiers in physiology · 2020Review
- LncRNA CASC2 inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation and migration by regulating the miR-222/ING5 axis.Cellular & molecular biology letters · 2020Article
- MiR145-5p inhibits proliferation of PMVECs via PAI-1 in experimental hepatopulmonary syndrome rat pulmonary microvascular hyperplasia.Biology open · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We have previously reported that miR-17~92 is critically involved in the pathogenesis of pulmonary hypertension (PH). We also identified two novel mR-17/20a direct targets, PDZ and LIM domain protein 5 (PDLIM5) and prolyl hydroxylase 2 (PHD2), and elucidated the signaling pathways by which PDLIM5 and PHD2 regulate functions of pulmonary artery smooth muscle cells (PASMCs). In addition, we have shown that plasminogen activator inhibitor-1 (PAI-1) is also downregulated in PASMCs that overexpress miR-17~92. However, it is unclear whether PAI-1 is a direct target of miR-17~92 and whether it plays a role in regulating the PASMC phenotype. In this study, we have identified PAI-1 as a novel target of miR-19a/b, two members of the miR-17~92 cluster. We found that the 3'-untranslated region (UTR) of PAI-1 contains a miR-19a/b binding site and that miR-19a/b can target this site to suppress PAI-1 protein expression. MiR-17/20a, two other members of miR-17~92, may also indirectly suppress PAI-1 expression through PDLIM5. PAI-1 is a negative regulator of miR-17~92-mediated PASMC proliferation. Silencing of PAI-1 induces Smad2/calponin signaling in PASMCs, suggesting that PAI-1 is a negative regulator of the PASMC contractile phenotype. We also found that PAI-1 is essential for the metabolic gene expression in PASMCs. Furthermore, although there is no significant change in PAI-1 levels in PASMCs isolated from idiopathic pulmonary arterial hypertension and associated pulmonary arterial hypertension patients, PAI-1 is downregulated in hypoxia/Sugen-induced hypertensive rat lungs. These results suggest that miR-17~92 regulates the PASMC contractile phenotype and proliferation coordinately and synergistically by direct and indirect targeting of PAI-1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.