Increase of macrophage migration inhibitory factor (MIF) expression in cardiomyocytes during chronic hypoxia
Zhao Jian1, Jia-Bei Li, Rui-Yan Ma
1Department of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University, 183 Xinqiao Street, Chongqing 400037, PR China.
Background:
Macrophage migration inhibitory factor (MIF) might play an important role in the myocardium during chronic hypoxia because MIF protects the heart during myocardial ischemia by activating 5'-adenosine monophosphate activated protein kinase (AMPK).
Methods:
We investigated 35 infants with cyanotic or acyanotic cardiac defects and H9c2 embryonic rat cardiomyocytes to examine the effect of chronic hypoxia on the expression of MIF in vivo and in vitro, respectively.
Results:
We found out an increase of endogenous cardiac MIF expression positively correlated with degree of hypoxia. Also, AMPK activation was elevated while MIF expression was increased in cells exposed to long periods of hypoxia in vitro. There was no significant difference in the growth ratio of cells cultivated in long periods of hypoxia and normoxia.
Conclusions:
The expression of MIF is significantly increased in cardiomyocytes exposed to chronic hypoxia, and the activation of AMPK was increased accordingly.
Insights
Chronic hypoxia increases macrophage migration inhibitory factor (MIF) in the heart, activating 5'-adenosine monophosphate activated protein kinase (AMPK). This finding is crucial for understanding heart adaptation to low oxygen conditions.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- Macrophage migration inhibitory factor (MIF) plays a role in myocardial adaptation to chronic hypoxia.
- MIF protects the heart during ischemia by activating 5'-adenosine monophosphate activated protein kinase (AMPK).
Purpose of the Study:
- To investigate the effect of chronic hypoxia on MIF expression in vivo and in vitro.
- To examine the relationship between MIF expression and AMPK activation under hypoxic conditions.
Main Methods:
- Studied 35 infants with congenital heart defects.
- Utilized H9c2 embryonic rat cardiomyocytes for in vitro experiments.
- Assessed MIF expression and AMPK activation under varying oxygen levels.
Main Results:
- Cardiac MIF expression increased with the degree of hypoxia in vivo.
- Hypoxia elevated MIF expression and AMPK activation in cardiomyocytes in vitro.
- Cell growth rates were similar in hypoxic and normoxic conditions.
Conclusions:
- MIF expression is significantly upregulated in cardiomyocytes under chronic hypoxia.
- AMPK activation increases in parallel with elevated MIF expression during hypoxia.
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