Phenylephrine-induced cardiac hypertrophy is attenuated by a histone acetylase inhibitor anacardic acid in mice

2017 ◽  
Vol 13 (4) ◽  
pp. 714-724 ◽  
Author(s):  
Chang Peng ◽  
Xiaomei Luo ◽  
Shuo Li ◽  
Huichao Sun
Keyword(s):  
Cardiac Hypertrophy ◽  
Anacardic Acid ◽  
Complex Process ◽  
Myocardium Remodeling

Cardiac hypertrophy is a complex process involving highly coordinated but tight regulation of multiple elements, such as in epigenetics, which make an important contribution to myocardium remodeling and cardiac hypertrophy.

scholarly journals Role of CyPA in cardiac hypertrophy and remodeling

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Mengfei Cao ◽  
Wei Yuan ◽  
Meiling Peng ◽  
Ziqi Mao ◽  
Qianru Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Interstitial Fibrosis ◽  
Systolic Function ◽  
Cardiac Fibroblasts ◽  
Cardiomyocyte Hypertrophy ◽  
Pathological Cardiac Hypertrophy ◽  
Complex Process

Abstract Pathological cardiac hypertrophy is a complex process and eventually develops into heart failure, in which the heart responds to various intrinsic or external stress, involving increased interstitial fibrosis, cell death and cardiac dysfunction. Studies have shown that oxidative stress is an important mechanism for this maladaptation. Cyclophilin A (CyPA) is a member of the cyclophilin (CyPs) family. Many cells secrete CyPA to the outside of the cells in response to oxidative stress. CyPA from blood vessels and the heart itself participate in a variety of signaling pathways to regulate the production of reactive oxygen species (ROS) and mediate inflammation, promote cardiomyocyte hypertrophy and proliferation of cardiac fibroblasts, stimulate endothelial injury and vascular smooth muscle hyperplasia, and promote the dissolution of extracellular matrix (ECM) by activating matrix metalloproteinases (MMPs). The events triggered by CyPA cause a decline of diastolic and systolic function and finally lead to the occurrence of heart failure. This article aims to introduce the role and mechanism of CyPA in cardiac hypertrophy and remodeling, and highlights its potential role as a disease biomarker and therapeutic target.

scholarly journals Anacardic acid protects against phenylephrine-induced mouse cardiac hypertrophy through JNK signaling-dependent regulation of histone acetylation

2020 ◽  
Author(s):  
Bohui Peng ◽  
Chang Peng ◽  
Xiaomei Luo ◽  
Lixin Huang ◽  
Qian Mao ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Histone Acetylation ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Anacardic Acid ◽  
Mitogen Activated Protein Kinase ◽  
Cardiomyocyte Hypertrophy ◽  
Jnk Signaling ◽  
Hat Inhibitor

AbstractCardiac hypertrophy is a complex process induced by the activation of multiple signaling pathways. We previously reported that anacardic acid (AA), a histone acetylase (HAT) inhibitor, attenuates phenylephrine (PE)-induced cardiac hypertrophy by downregulating histone H3 acetylation at lysine 9 (H3K9ac). Unfortunately, the upstream signaling events remained unknown. The mitogen-activated protein kinase (MAPK) pathway is an important regulator of cardiac hypertrophy. In this study, we explored the role of JNK/MAPK signaling in cardiac hypertrophy. A mouse model of cardiomyocyte hypertrophy was successfully established in vitro using PE. This study showed that p-JNK directly interacts with HATs (P300 and P300/CBP-associated factor, PCAF) and alters H3K9ac. In addition, both the JNK inhibitor SP600125 and the HAT inhibitor AA attenuated p-JNK overexpression and H3K9 hyperacetylation by inhibiting P300 and PCAF during PE-induced cardiomyocyte hypertrophy. Moreover, we demonstrated that both SP600125 and AA attenuate the overexpression of cardiac hypertrophy-related genes (MEF2A, ANP, BNP, and β-MHC), preventing cardiomyocyte hypertrophy and dysfunction. These results revealed a novel mechanism through which AA might protect mice from PE-induced cardiac hypertrophy. In particular, AA inhibits the effects of JNK signaling on HAT-mediated histone acetylation, and could therefore be used to prevent and treat hypertrophic cardiomyopathy.

scholarly journals JNK signaling-dependent regulation of histone acetylation are involved in anacardic acid alleviates cardiomyocyte hypertrophy induced by phenylephrine

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261388
Author(s):  
Bohui Peng ◽  
Chang Peng ◽  
Xiaomei Luo ◽  
Shuqi Wu ◽  
Qian Mao ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Histone Acetylation ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Anacardic Acid ◽  
Mitogen Activated Protein Kinase ◽  
Cardiomyocyte Hypertrophy ◽  
Jnk Signaling ◽  
Hat Inhibitor

Cardiac hypertrophy is a complex process induced by the activation of multiple signaling pathways. We previously reported that anacardic acid (AA), a histone acetyltransferase (HAT) inhibitor, attenuates phenylephrine (PE)-induced cardiac hypertrophy by downregulating histone H3 acetylation at lysine 9 (H3K9ac). Unfortunately, the related upstream signaling events remained unknown. The mitogen-activated protein kinase (MAPK) pathway is an important regulator of cardiac hypertrophy. In this study, we explored the role of JNK/MAPK signaling pathway in cardiac hypertrophy induced by PE. The mice cardiomyocyte hypertrophy model was successfully established by treating cells with PE in vitro. This study showed that p-JNK directly interacts with HATs (P300 and P300/CBP-associated factor, PCAF) and alters H3K9ac. In addition, both the JNK inhibitor SP600125 and the HAT inhibitor AA attenuated p-JNK overexpression and H3K9ac hyperacetylation by inhibiting P300 and PCAF during PE-induced cardiomyocyte hypertrophy. Moreover, we demonstrated that both SP600125 and AA attenuate the overexpression of cardiac hypertrophy-related genes (MEF2A, ANP, BNP, and β-MHC), preventing cardiomyocyte hypertrophy and dysfunction. These results revealed a novel mechanism through which AA might protect mice from PE-induced cardiomyocyte hypertrophy. In particular, AA inhibits the effects of JNK signaling on HATs-mediated histone acetylation, and could therefore be used to prevent and treat pathological cardiac hypertrophy.

scholarly journals Anacardic acid attenuates pressure‐overload cardiac hypertrophy through inhibiting histone acetylases

2019 ◽  
Vol 23 (4) ◽  
pp. 2744-2752 ◽  
Author(s):  
Shuo Li ◽  
Bohui Peng ◽  
Xiaomei Luo ◽  
Huichao Sun ◽  
Chang Peng
Keyword(s):  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Anacardic Acid ◽  
Histone Acetylases

Alcohol-induced histone H3K9 hyperacetylation and cardiac hypertrophy are reversed by a histone acetylases inhibitor anacardic acid in developing murine hearts

Biochimie ◽  
2015 ◽  
Vol 113 ◽  
pp. 1-9 ◽  
Author(s):  
Chang Peng ◽  
Weihua Zhang ◽  
Weian Zhao ◽  
Jing Zhu ◽  
Xupei Huang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Anacardic Acid ◽  
Histone Acetylases

ultrastructural process of intestinal wound healing

1995 ◽  
Vol 53 ◽  
pp. 1024-1025
Author(s):  
Rick L. Vaughn ◽  
Shailendra K. Saxena ◽  
John G. Sharp
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Smooth Muscles ◽  
Microscopic Level ◽  
Light Microscopic Level ◽  
Ileal Mucosa ◽  
Wound Model ◽  
Serosal Surface ◽  
Complex Process ◽  
Orderly Fashion

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.

421 The NFATc2 isoform plays a major role in calcineurin-induced cardiac hypertrophy

2006 ◽  
Vol 5 (1) ◽  
pp. 98-98
Author(s):  
M BOURAJJAJ ◽  
A ARMAND ◽  
B WEIJTS ◽  
L DEWINDT
Keyword(s):  
Cardiac Hypertrophy

Sex differences in cardiac hypertrophy are linked to adipose tissue lipolysis

2011 ◽  
Vol 6 (S 01) ◽  
Author(s):  
A Foryst-Ludwig ◽  
M Kreissl ◽  
C Sprang ◽  
B Thalke ◽  
C Böhm ◽  
...  
Keyword(s):  
Sex Differences ◽  
Adipose Tissue ◽  
Cardiac Hypertrophy ◽  
Adipose Tissue Lipolysis

Adventism in Ukraine: Attitude to national and cultural traditions, phenomena of the present

1997 ◽  
pp. 33-36
Author(s):  
Anatoliy Moskovchuk
Keyword(s):  
Cultural Heritage ◽  
Cultural Traditions ◽  
National Minorities ◽  
Complex Process ◽  
Different Cultures ◽  
Historical Contribution ◽  
Intellectual Environment

Ukraine is the motherland of not only Ukrainians but also of many national minorities with different cultures and traditions. Ukraine is a Christian country in general, with non-Christian and non-Christian religions and confessional currents, along with traditional churches - Orthodox, Catholic, Protestant - rooted and actively developing non-traditional Ukrainian culture and spirituality. In Ukraine there is a complex process of spiritual revival, especially in the intellectual environment. Many are written and talk about the preservation of cultural heritage. Everywhere, monuments of architecture, art, which testify to the generally recognized historical contribution of Christianity to the development of spirituality and morality of the Ukrainian people, are restored. In our eyes, there are changes in social and religious relations.

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