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Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice

This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We establish...

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Autores principales: Yang, Yongyao, Tang, Feng, Wei, Fang, Yang, Long, Kuang, Chunyan, Zhang, Hongming, Deng, Jiusheng, Wu, Qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914395/
https://www.ncbi.nlm.nih.gov/pubmed/31757932
http://dx.doi.org/10.18632/aging.102388
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author Yang, Yongyao
Tang, Feng
Wei, Fang
Yang, Long
Kuang, Chunyan
Zhang, Hongming
Deng, Jiusheng
Wu, Qiang
author_facet Yang, Yongyao
Tang, Feng
Wei, Fang
Yang, Long
Kuang, Chunyan
Zhang, Hongming
Deng, Jiusheng
Wu, Qiang
author_sort Yang, Yongyao
collection PubMed
description This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression. H19 was capable of recruiting CTCF to suppress PKD1, thus promoting atherosclerotic vulnerable plaque formation and intraplaque angiogenesis in atherosclerosis mice. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis.
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spelling pubmed-69143952019-12-19 Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice Yang, Yongyao Tang, Feng Wei, Fang Yang, Long Kuang, Chunyan Zhang, Hongming Deng, Jiusheng Wu, Qiang Aging (Albany NY) Research Paper This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression. H19 was capable of recruiting CTCF to suppress PKD1, thus promoting atherosclerotic vulnerable plaque formation and intraplaque angiogenesis in atherosclerosis mice. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis. Impact Journals 2019-11-22 /pmc/articles/PMC6914395/ /pubmed/31757932 http://dx.doi.org/10.18632/aging.102388 Text en Copyright © 2019 Yang et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Yang, Yongyao
Tang, Feng
Wei, Fang
Yang, Long
Kuang, Chunyan
Zhang, Hongming
Deng, Jiusheng
Wu, Qiang
Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title_full Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title_fullStr Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title_full_unstemmed Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title_short Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
title_sort silencing of long non-coding rna h19 downregulates ctcf to protect against atherosclerosis by upregulating pkd1 expression in apoe knockout mice
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914395/
https://www.ncbi.nlm.nih.gov/pubmed/31757932
http://dx.doi.org/10.18632/aging.102388
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