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SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17

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 mode...

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Autores principales: Long, Yadong, Wang, Lin, Li, Zhiqiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339172/
https://www.ncbi.nlm.nih.gov/pubmed/32436661
http://dx.doi.org/10.1111/jcmm.15073
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author Long, Yadong
Wang, Lin
Li, Zhiqiang
author_facet Long, Yadong
Wang, Lin
Li, Zhiqiang
author_sort Long, Yadong
collection PubMed
description 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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spelling pubmed-73391722020-07-13 SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17 Long, Yadong Wang, Lin Li, Zhiqiang J Cell Mol Med Original Articles 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. John Wiley and Sons Inc. 2020-05-21 2020-07 /pmc/articles/PMC7339172/ /pubmed/32436661 http://dx.doi.org/10.1111/jcmm.15073 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Long, Yadong
Wang, Lin
Li, Zhiqiang
SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title_full SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title_fullStr SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title_full_unstemmed SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title_short SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17
title_sort sp1‐induced snhg14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of pcdh17
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339172/
https://www.ncbi.nlm.nih.gov/pubmed/32436661
http://dx.doi.org/10.1111/jcmm.15073
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AT lizhiqiang sp1inducedsnhg14aggravateshypertrophicresponseininvitromodelofcardiachypertrophyviaupregulationofpcdh17