Ascorbic Acid Protects against Hypertension through Downregulation of ACE1 Gene Expression Mediated by Histone Deacetylation in Prenatal Inflammation-Induced Offspring

Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. However, the mechanism is still unclear. This study unraveled epigenetic mechanism for this and explored the protective effects...

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Published inScientific reports Vol. 6; no. 1; p. 39469
Main Authors Wang, Jing, Yin, Na, Deng, Youcai, Wei, Yanling, Huang, Yinhu, Pu, Xiaoyun, Li, Li, Zheng, Yingru, Guo, Jianxin, Yu, Jianhua, Li, Xiaohui, Yi, Ping
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 20.12.2016
Nature Publishing Group
Subjects
38/15
38/90
631/136/2442
64
692/699/75/243
82
82/1
82/29
82/80
Ace1 gene
Acetylation
Acids
Angiotensin
Ascorbic acid
Cardiovascular diseases
Deacetylation
Fetuses
Gene expression
Histone H3
Humanities and Social Sciences
Hypertension
Inflammation
Lipopolysaccharides
multidisciplinary
Offspring
Oxidative stress
Peptidyl-dipeptidase A
Prenatal experience
Prenatal exposure
Rodents
Science
Vitamin C
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Abstract Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. However, the mechanism is still unclear. This study unraveled epigenetic mechanism for this and explored the protective effects of ascorbic acid against hypertension on prenatal inflammation-induced offspring. Prenatal LPS exposure resulted in an increase of intrarenal oxidative stress and enhanced angiotensin-converting enzyme 1 ( ACE1 ) gene expression at the mRNA and protein levels in 6- and 12-week-old offspring, correlating with the augmentation of histone H3 acetylation (H3AC) on the ACE1 promoter. However, the prenatal ascorbic acid treatment decreased the LPS-induced expression of ACE1 , protected against intrarenal oxidative stress, and reversed the altered histone modification on the ACE1 promoter, showing the protective effect in offspring of prenatal LPS stimulation. Our study demonstrates that ascorbic acid is able to prevent hypertension in offspring from prenatal inflammation exposure. Thus, ascorbic acid can be a new approach towards the prevention of fetal programming hypertension.
AbstractList Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. However, the mechanism is still unclear. This study unraveled epigenetic mechanism for this and explored the protective effects of ascorbic acid against hypertension on prenatal inflammation-induced offspring. Prenatal LPS exposure resulted in an increase of intrarenal oxidative stress and enhanced angiotensin-converting enzyme 1 (ACE1) gene expression at the mRNA and protein levels in 6- and 12-week-old offspring, correlating with the augmentation of histone H3 acetylation (H3AC) on the ACE1 promoter. However, the prenatal ascorbic acid treatment decreased the LPS-induced expression of ACE1, protected against intrarenal oxidative stress, and reversed the altered histone modification on the ACE1 promoter, showing the protective effect in offspring of prenatal LPS stimulation. Our study demonstrates that ascorbic acid is able to prevent hypertension in offspring from prenatal inflammation exposure. Thus, ascorbic acid can be a new approach towards the prevention of fetal programming hypertension.
Abstract Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. However, the mechanism is still unclear. This study unraveled epigenetic mechanism for this and explored the protective effects of ascorbic acid against hypertension on prenatal inflammation-induced offspring. Prenatal LPS exposure resulted in an increase of intrarenal oxidative stress and enhanced angiotensin-converting enzyme 1 ( ACE1 ) gene expression at the mRNA and protein levels in 6- and 12-week-old offspring, correlating with the augmentation of histone H3 acetylation (H3AC) on the ACE1 promoter. However, the prenatal ascorbic acid treatment decreased the LPS-induced expression of ACE1 , protected against intrarenal oxidative stress, and reversed the altered histone modification on the ACE1 promoter, showing the protective effect in offspring of prenatal LPS stimulation. Our study demonstrates that ascorbic acid is able to prevent hypertension in offspring from prenatal inflammation exposure. Thus, ascorbic acid can be a new approach towards the prevention of fetal programming hypertension.
Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. However, the mechanism is still unclear. This study unraveled epigenetic mechanism for this and explored the protective effects of ascorbic acid against hypertension on prenatal inflammation-induced offspring. Prenatal LPS exposure resulted in an increase of intrarenal oxidative stress and enhanced angiotensin-converting enzyme 1 ( ACE1 ) gene expression at the mRNA and protein levels in 6- and 12-week-old offspring, correlating with the augmentation of histone H3 acetylation (H3AC) on the ACE1 promoter. However, the prenatal ascorbic acid treatment decreased the LPS-induced expression of ACE1 , protected against intrarenal oxidative stress, and reversed the altered histone modification on the ACE1 promoter, showing the protective effect in offspring of prenatal LPS stimulation. Our study demonstrates that ascorbic acid is able to prevent hypertension in offspring from prenatal inflammation exposure. Thus, ascorbic acid can be a new approach towards the prevention of fetal programming hypertension.
ArticleNumber 39469
Author Li, Li
Zheng, Yingru
Guo, Jianxin
Yi, Ping
Deng, Youcai
Li, Xiaohui
Pu, Xiaoyun
Yu, Jianhua
Wang, Jing
Wei, Yanling
Yin, Na
Huang, Yinhu
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Snippet Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a...
Abstract Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Prenatal exposure to lipopolysaccharide (LPS) leads to...
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SubjectTerms 38/15
38/90
631/136/2442
64
692/699/75/243
82
82/1
82/29
82/80
Ace1 gene
Acetylation
Acids
Angiotensin
Ascorbic acid
Cardiovascular diseases
Deacetylation
Fetuses
Gene expression
Histone H3
Humanities and Social Sciences
Hypertension
Inflammation
Lipopolysaccharides
multidisciplinary
Offspring
Oxidative stress
Peptidyl-dipeptidase A
Prenatal experience
Prenatal exposure
Rodents
Science
Vitamin C
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Title Ascorbic Acid Protects against Hypertension through Downregulation of ACE1 Gene Expression Mediated by Histone Deacetylation in Prenatal Inflammation-Induced Offspring
URI https://link.springer.com/article/10.1038/srep39469
https://www.ncbi.nlm.nih.gov/pubmed/27995995
https://www.proquest.com/docview/1899430793
https://search.proquest.com/docview/1851299146
https://pubmed.ncbi.nlm.nih.gov/PMC5171640
Volume 6
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