Annexins, calcium-dependent phospholipid binding proteins in irreducible heart failure
T Branishte1, Catalina Arsenescu-Georgescu2, Mirela-Cleopatra Tomescu3
1State Medical and Pharmaceutical University "Nicolae Testemitanu", Chisinau,
Insights
Heart failure patients show increased annexin V and VI levels in heart muscle. These proteins redistribute from cell membranes to the interstitium in dilated cardiomyopathy, suggesting a role in heart failure pathogenesis.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Protein Biochemistry
Background:
- Annexins are calcium-dependent phospholipid-binding proteins.
- Annexins V and VI play roles in membrane structure and signaling.
- Their function in human heart failure is not fully understood.
Purpose of the Study:
- To investigate the expression and distribution of annexins V and VI.
- To compare intact human hearts with dilated cardiomyopathy (DCM) hearts.
- To elucidate the role of annexins in heart failure pathogenesis.
Main Methods:
- Studied left ventricular myocardium from nine DCM patients and nine controls.
- Utilized immunoblotting and indirect immunofluorescence.
- Quantified annexin levels and determined their cellular localization.
Main Results:
- Annexins V and VI levels were significantly increased (122% and 119%) in DCM myocardium.
- In healthy hearts, annexin V localized to sarcolemma and intercalated discs.
- In DCM, annexins V and VI were found in the interstitium, with annexin V also at the sarcolemma.
Conclusions:
- Annexin V and VI expression is upregulated in DCM.
- Redistribution of annexins V and VI to the interstitium occurs in heart failure.
- These changes suggest disturbed myocardial protein expression contributes to heart failure.
Aim:
To analyze the expression and distribution of annexins V and VI in intact human hearts and in dilated cardiomyopathy (DCM) in patients with irreducible heart failure.
Material And Methods:
The study included nine patients with DCM and irreducible heart failure. By immunoblotting and indirect immunofluorescence, the amount and location of annexins was determined using samples of left ventricular (LV) myocardium collected during orthotopic heart allotransplantation. Samples of LV myocardium from 9 individuals who died of craniocerebral trauma served as controls.
Results:
Quantitative analysis showed an increased level of both annexins in the myocardium of DCM patients compared with normal myocardium: 122 +/- 5% (p < 0.05) and 119 +/- 5% (p < 0.05) for annexins V and VI, respectively. In the intact heart annexin V was located at the sarcolemma and intercalated discs, while in the myocardium with heart failure mainly in the interstitium. In normal hearts, annexin VI was located at the sarcolema, including T-tubules, Z-lines and intercalated discs. In heart failure, annexin V1 was also located in the interstitium.
Conclusions:
Redistribution of annexins V and VI in the cardiomyocytes in the interstitial space may have important functional consequences and indicates the role of myocardial protein expression disturbances in the etiology and/or pathogenesis of heart failure in pa-
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