ArticleJournal of cellular and molecular medicine2020
SP1-induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up-regulation of PCDH17.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- The molecular and cellular landscape of hypertrophic cardiomyopathy phenotypes: transition from obstructive to end-stage heart failure.Journal of molecular medicine (Berlin, Germany) · 2025Pooled it
- METTL3 Confers Ischemia/Reperfusion-Caused Myocardial Injury by Triggering Ferroptosis via Regulating the lncRNA SNHG14/miR-195a-5p/ACSL4 Axis.Cardiovascular drugs and therapy · 2026Article
- Embedding multilayer RNA networks for lncRNA-miRNA interaction prediction via LMI-MHGAT.BMC biology · 2026Article
- Unlocking the life code: a review of SnoRNA functional diversity and disease relevance.Cell communication and signaling : CCS · 2025Review
- Construction of a competitive endogenous RNA network and identification of potential regulatory axes in hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy.Protein & cell · 2024Article
- Identification of hub lncRNAs correlated with tetralogy of fallot based on weighted gene co-expression network analysis.Biochemistry and biophysics reports · 2024Article
- Role of Specificity Protein 1 (SP1) in Cardiovascular Diseases: Pathological Mechanisms and Therapeutic Potentials.Biomolecules · 2024Review
- Plac8-ERK pathway modulation of monocyte function in sepsis.Cell death discovery · 2024Article
- MicroRNA-322-5p targeting Smurf2 regulates the TGF-β/Smad pathway to protect cardiac function and inhibit myocardial infarction.Human cell · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
- SLC26A4-AS1 Aggravates AngII-induced Cardiac Hypertrophy by Enhancing SLC26A4 Expression.Arquivos brasileiros de cardiologia · 2023Article
- Upregulated miR-322-5p regulates cell cycle and promotes cell proliferation and apoptosis by directly targeting Wee1 in mice liver injury.Cell cycle (Georgetown, Tex.) · 2022Article
- lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.Bioengineered · 2022Article
- Hypermethylation-Mediated Silencing ofInternational journal of molecular sciences · 2022Article
- MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5.Yonsei medical journal · 2022Article
- Article
- Global RNA editing identification and characterization during human pluripotent-to-cardiomyocyte differentiation.Molecular therapy. Nucleic acids · 2021Article
- The function of LncRNA-H19 in cardiac hypertrophy.Cell & bioscience · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy (CH) is a common cardiac disease and is closely associated with heart failure. Protocadherin 17 (PCDH17) was reported to aggravate myocardial infarction. Present study was designed to illustrate the impact of PCDH17 and the mechanism of PCDH17 expression regulation in CH. CH model in vivo and in vitro was established by transverse aortic constriction (TAC) and Ang-II treatment. Hypertrophy was evaluated in PMC and H9c2 cells by examining cell surface area and hypertrophic markers. Results demonstrated that PCDH17 was up-regulated in CH in vivo and in vitro. PCDH17 knock-down alleviated hypertrophic response in Ang-II-induced cardiomyocytes. By means of ENCORI database and a series of mechanism assays, miR-322-5p and miR-384-5p were identified to interact with and inhibit PCDH17. Next, lncRNA SNHG14 (small nucleolar RNA host gene 14) was validated to sponge both miR-322-5p and miR-384-5p to elevate PCDH17 level. The subsequent rescue assays revealed that miR-322-5p and miR-384-5p restored SNHG14 depletion-mediated suppression on hypertrophy in Ang-II-induced cardiomyocytes. Besides, Sp1 transcription factor (SP1) was verified as the transcription factor activating both SNHG14 and PCDH17. Both SNHG14 and PCDH17 reversed SP1 knock-down-mediated repression on hypertrophy in Ang-II-induced cardiomyocytes. Together, present study first uncovered ceRNA network of SNHG14/miR-322-5p/miR-384-5p/PCDH17 in Ang-II-induced cardiomyocytes.
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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.