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Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway
Jayeeta Samanta1, Arunima Mondal1, Srimoyee Saha2
1Department of Life science and Biotechnology, Jadavpur University, 188, Raja S. C. Mallick Road, Kolkata, West Bengal, 700032, India.
Abstract:
Arsenic toxicity is one of the major environmental problems causing various diseases, cardiovascular disorders is one of them. Several epidemiological studies have shown that arsenic causes cardiac hypertrophy but the detailed molecular mechanism is to be studied yet. This study is designed to determine the molecules involved in the augmentation of arsenic-induced cardiac hypertrophy. Furthermore, the effects of oleic acid on arsenic-induced hypertrophy and cardiac injury have also been investigated. Our results show that arsenic induces cardiac hypertrophy both in vivo in mice and in vitro in rat H9c2 cardiomyocytes. Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer. In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells. Interestingly, we have observed that oleic acid helps in ameliorating cardiac hypertrophy in arsenic-exposed mice. Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy. This study will help in finding out new avenues in treating arsenic-induced cardiac hypertrophy.
Insights
Arsenic exposure causes cardiac hypertrophy by altering key molecular pathways. Oleic acid shows promise in protecting against this arsenic-induced heart condition by restoring molecular balance.
Area of Science:
- Environmental toxicology
- Cardiovascular research
- Molecular mechanisms of disease
Background:
- Arsenic toxicity is a significant environmental health concern linked to cardiovascular disorders.
- Epidemiological studies suggest arsenic exposure contributes to cardiac hypertrophy, but underlying molecular mechanisms require elucidation.
- Understanding these mechanisms is crucial for developing targeted therapeutic strategies.
Purpose of the Study:
- To identify molecular players involved in arsenic-induced cardiac hypertrophy.
- To investigate the protective effects of oleic acid against arsenic-induced cardiac hypertrophy and injury.
- To explore the role of AMPK, FoxO1, and NFATc3 in arsenic toxicity and oleic acid's ameliorating effects.
Main Methods:
- In vivo studies using mice exposed to arsenic.
- In vitro studies using rat H9c2 cardiomyocytes exposed to arsenic.
- Assays to measure enzyme activity (AMPK), protein localization (FoxO1), and gene expression (NFATc3).
Main Results:
- Arsenic exposure induced cardiac hypertrophy in both in vivo and in vitro models.
- Arsenic decreased AMPK and FoxO1 activity while increasing NFATc3 expression.
- Oleic acid administration ameliorated arsenic-induced cardiac hypertrophy by activating AMPK, promoting FoxO1 nuclear localization, and reducing NFATc3 expression.
Conclusions:
- Arsenic-induced cardiac hypertrophy involves the dysregulation of AMPK, FoxO1, and NFATc3 pathways.
- Activation of AMPK and FoxO1 plays a protective role by inhibiting NFATc3 and attenuating hypertrophy.
- Oleic acid demonstrates therapeutic potential for mitigating arsenic-induced cardiac hypertrophy, offering new treatment avenues.
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