ArticleJournal of clinical laboratory analysis2022
Decrease in LINC00963 attenuates the progression of pulmonary arterial hypertension via microRNA-328-3p/profilin 1 axis.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- LINC00963 targeting miR-98-5p exacerbates sepsis-induced myocardial injury.Internal and emergency medicine · 2026Article
- Review
- miRNA regulatory networks as precision diagnostic and therapeutic targets in pulmonary arterial hypertension: from molecular cascades to clinical translation.American journal of cardiovascular disease · 2025Review
- Biomarkers in COPD-Associated PH/CCP: Circulating Molecules and Cell-Intrinsic Marker.International journal of chronic obstructive pulmonary disease · 2025Review
- Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024Review
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Unraveling the role of HIF and epigenetic regulation in pulmonary arterial hypertension: implications for clinical research and its therapeutic approach.Frontiers in medicine · 2024Review
- Genetic and epigenetic factors of arterial hypertension: a bibliometric- and in-silico-based analyses.Frontiers in molecular biosciences · 2023Review
- Construction and Comprehensive Analysis of miRNAs and Target mRNAs inLife (Basel, Switzerland) · 2022Article
- Decrease in LINC00963 attenuates the progression of pulmonary arterial hypertension via microRNA-328-3p/profilin 1 axis.Journal of clinical laboratory analysis · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary arterial hypertension (PAH) is a severe cardiopulmonary disease characterized by vascular hyperplasia and remodeling. Long noncoding RNA LINC00963 can regulate cell proliferation and metastasis in nonsmall cell lung cancer. However, the function of LINC00963 on PAH progression is rarely reported.
methodsQuantitative real-time PCR was used to determine the expression levels of LINC00963, microRNA (miRNA)-328-3p, and profilin 1 (PFN1), as well as vascular endothelial growth factor (VEGF), fibroblast growth factor 2 (FGF-2), and hypoxia-inducible factor (HIF)-α. The protein level of PFN1 was measured by western blotting. The viability and migration of hypoxia-induced pulmonary arterial smooth muscle cells (PASMCs) were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-h-tetrazolium bromide, and transwell assays, respectively. The target relationships between miR-328-3p and LINC00963/PFN1 were confirmed by dual-luciferase reporter assay. A PAH mouse model was conducted to explore the effects of hypoxia on cardiopulmonary functions.
resultsIn hypoxia-induced PASMCs and PAH mouse model, high expression levels of LINC00963 and PFN1, and low expression of miR-328-3p, were determined. The viability, migration of hypoxia-induced PASMCs, the expression of VEGF, FGF-2, and HIF-α were significantly repressed by transfection of si-LINC00963 or miR-328-3p mimics. The inhibitory effects of LINC00963 silencing on cell viability, migration, and the levels of VEGF, FGF-2, and HIF-α were partly eliminated by miR-328-3p inhibitor or increasing the expression of PFN1. Hypoxia treatment increased the levels of RVSP, mPAP, and RV/(LV+S), as well as the thickness of pulmonary artery wall.
conclusionsSilencing of LINC00963 ameliorates PAH via modulating miR-328-3p/PFN1.
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