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Increased myocardial GRP94 amounts during sustained atrial fibrillation: a protective response?
M Vitadello1, J Ausma, M Borgers
1CNR Unit for Muscle Physiology and Physiopathology, Department of Biomedical Sciences, University of Padova, Padova, Italy.
Circulation
|May 23, 2001
Summary
Chronic atrial fibrillation leads to increased glucose-regulated protein GRP94 in heart cells. This GRP94 increase is reversible, suggesting a protective cellular response in fibrillating atria.
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Molecular Cardiology
Background:
- Atrial fibrillation is associated with structural and phenotypic changes in cardiomyocytes.
- Glucose-regulated protein GRP94 is crucial for cell viability and its role in atrial fibrillation is unclear.
Purpose of the Study:
- To investigate changes in GRP94 expression in atrial cardiomyocytes during chronic atrial fibrillation.
- To determine if GRP94 levels are altered in human and animal models of atrial fibrillation.
Main Methods:
- Analysis of GRP94 expression in atrial myocardium from goats and humans using immunologic approaches.
- Induction and maintenance of atrial fibrillation in goats for up to 16 weeks, followed by cardioversion.
- Immunohistochemical analysis to confirm the location of GRP94 increase within cardiomyocytes.
Main Results:
- GRP94 levels doubled in goat atrial myocytes after 4-16 weeks of fibrillation, returning to normal after cardioversion.
- Increased GRP94 was also observed in human fibrillating atrial samples.
- Unlike calreticulin, inducible HSP70 increased in fibrillating atria, suggesting a stress response.
Conclusions:
- A significant, reversible increase in GRP94 occurs in atrial myocytes during chronic atrial fibrillation.
- This GRP94 upregulation may represent a protective cellular mechanism in response to fibrillation.
- The findings highlight GRP94's potential role in the adaptive response of cardiomyocytes to stress.
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