Cargando…
Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway
Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload....
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Ivyspring International Publisher
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738963/ https://www.ncbi.nlm.nih.gov/pubmed/33390770 http://dx.doi.org/10.7150/ijms.51133 |
_version_ | 1783623231626805248 |
---|---|
author | Wang, Jinghao Hao, Dan Zeng, Lingfeng Zhang, Qianhui Huang, Wei |
author_facet | Wang, Jinghao Hao, Dan Zeng, Lingfeng Zhang, Qianhui Huang, Wei |
author_sort | Wang, Jinghao |
collection | PubMed |
description | Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload. Abdominal aortic constriction (AAC) was used to induce CH model in rats. NPY or angiotensin II (Ang II) was used to trigger CH model in vitro in neonatal rat ventricular myocytes (NRVMs). We found that NPY was increased in the heart and plasma of hypertrophic rats. However, Ang II did not increase NPY expression in cardiomyocytes. NPY-I attenuated CH as decreasing CH-related markers (ANP, BNP and β-MHC mRNA) level, reducing cell surface area, and restoring cardiac function. NPY inactivation increased miR-216b and decreased FoxO4 expression in CH heart. Moreover, NPY decreased miR-216b and increased FoxO4 expression in NRVMs which were reversed by NPY type 1 receptor (NPY1R) antagonist BIBO3304. MiR-216b mimic and FoxO4 siRNA (small interfering RNA) inhibited NPY/Ang II-induced myocardial hypertrophy in vitro. Meanwhile, BIBO3304 reversed the pro-hypertrophy effect of NPY in vitro. Collectively, NPY deficiency attenuated CH by NPY1R-miR-216b-FoxO4 axis. These findings suggested that NPY would be a potential therapeutic target for the prevention and treatment of cardiac hypertrophy. |
format | Online Article Text |
id | pubmed-7738963 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-77389632021-01-01 Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway Wang, Jinghao Hao, Dan Zeng, Lingfeng Zhang, Qianhui Huang, Wei Int J Med Sci Research Paper Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload. Abdominal aortic constriction (AAC) was used to induce CH model in rats. NPY or angiotensin II (Ang II) was used to trigger CH model in vitro in neonatal rat ventricular myocytes (NRVMs). We found that NPY was increased in the heart and plasma of hypertrophic rats. However, Ang II did not increase NPY expression in cardiomyocytes. NPY-I attenuated CH as decreasing CH-related markers (ANP, BNP and β-MHC mRNA) level, reducing cell surface area, and restoring cardiac function. NPY inactivation increased miR-216b and decreased FoxO4 expression in CH heart. Moreover, NPY decreased miR-216b and increased FoxO4 expression in NRVMs which were reversed by NPY type 1 receptor (NPY1R) antagonist BIBO3304. MiR-216b mimic and FoxO4 siRNA (small interfering RNA) inhibited NPY/Ang II-induced myocardial hypertrophy in vitro. Meanwhile, BIBO3304 reversed the pro-hypertrophy effect of NPY in vitro. Collectively, NPY deficiency attenuated CH by NPY1R-miR-216b-FoxO4 axis. These findings suggested that NPY would be a potential therapeutic target for the prevention and treatment of cardiac hypertrophy. Ivyspring International Publisher 2021-01-01 /pmc/articles/PMC7738963/ /pubmed/33390770 http://dx.doi.org/10.7150/ijms.51133 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper Wang, Jinghao Hao, Dan Zeng, Lingfeng Zhang, Qianhui Huang, Wei Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title | Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title_full | Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title_fullStr | Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title_full_unstemmed | Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title_short | Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway |
title_sort | neuropeptide y mediates cardiac hypertrophy through microrna-216b/foxo4 signaling pathway |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738963/ https://www.ncbi.nlm.nih.gov/pubmed/33390770 http://dx.doi.org/10.7150/ijms.51133 |
work_keys_str_mv | AT wangjinghao neuropeptideymediatescardiachypertrophythroughmicrorna216bfoxo4signalingpathway AT haodan neuropeptideymediatescardiachypertrophythroughmicrorna216bfoxo4signalingpathway AT zenglingfeng neuropeptideymediatescardiachypertrophythroughmicrorna216bfoxo4signalingpathway AT zhangqianhui neuropeptideymediatescardiachypertrophythroughmicrorna216bfoxo4signalingpathway AT huangwei neuropeptideymediatescardiachypertrophythroughmicrorna216bfoxo4signalingpathway |