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Published on: May 28, 2019
Arginase 1 is upregulated at admission in patients with ST-elevation myocardial infarction
John Tengbom1, Sofia Cederström2, Dinos Verouhis1
1Unit of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Insights
Arginase 1 gene and protein expression significantly increase in ST-elevation myocardial infarction (STEMI) patients upon admission, suggesting its role in heart attack development. Levels remain elevated for months, but don't correlate with infarct size.
Area of Science:
- Cardiovascular biology
- Molecular mechanisms of myocardial infarction
Background:
- ST-elevation myocardial infarction (STEMI) pathogenesis, including plaque rupture and ischemia-reperfusion injury, is not fully understood.
- Increased arginase 1 activity impairs nitric oxide (NO) production and promotes reactive oxygen species, leading to endothelial dysfunction and plaque instability.
Purpose of the Study:
- To investigate the hypothesis that arginase gene and protein expression are upregulated in STEMI patients.
Main Methods:
- Two patient cohorts with STEMI were analyzed.
- Gene and protein expression of arginase and nitric oxide synthases were measured.
- Plasma arginase 1 levels and infarct size were assessed using cardiac magnetic resonance imaging.
Main Results:
- Arginase 1 gene expression was significantly elevated at admission and 24-48 hours post-STEMI, returning to baseline by 3 months.
- Arginase 1 protein levels were elevated upon admission and remained high for up to 6 months.
- No significant correlation was found between plasma arginase 1 levels and infarct size.
Conclusions:
- Elevated arginase 1 gene and protein expression at admission suggests a significant role in STEMI development.
- Arginase 1 is implicated in the acute phase of STEMI, with sustained protein elevation.
Background:
The mechanisms underlying rupture of a coronary atherosclerotic plaque and development of myocardial ischemia-reperfusion injury in ST-elevation myocardial infarction (STEMI) remain unresolved. Increased arginase 1 activity leads to reduced nitric oxide (NO) production and increased formation of reactive oxygen species due to uncoupling of the NO-producing enzyme endothelial NO synthase (eNOS). This contributes to endothelial dysfunction, plaque instability and increased susceptibility to ischemia-reperfusion injury in acute myocardial infarction.
Objective:
The purpose of this study was to test the hypothesis that arginase gene and protein expression are upregulated in patients with STEMI.
Methods:
Two cohorts of patients with STEMI were included. In the first cohort (n = 51), expression of arginase and NO-synthases as well as arginase 1 protein levels were determined and compared to a healthy control group (n = 45). In a second cohort (n = 68), plasma arginase 1 levels and infarct size were determined using cardiac magnetic resonance imaging.
Results:
Expression of the gene encoding arginase 1 was significantly elevated at admission and 24-48 h after STEMI but not 3 months post STEMI, in comparison with the control group. Expression of the genes encoding arginase 2 and endothelial NO synthase (NOS3) were unaltered. Arginase 1 protein levels were elevated at admission, 24 h post STEMI and remained elevated for up to 6 months. No significant correlation between plasma arginase 1 protein levels and infarct size was observed.
Conclusion:
The markedly increased gene and protein expression of arginase 1 already at admission indicates a role of arginase 1 in the development of STEMI.
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