| Decreased myocardial chromogranin a expression and colocalization with brain natriuretic peptide during reverse cardiac remodeling after ventricular unloading. | |
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MedLine Citation:
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PMID: 18374882 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS: In chronic heart failure, atrial and brain natriuretic peptide expression is increased and serves as a clinical marker of cardiac hypertrophy. Chromogranin A is also up-regulated during chronic heart failure and associated with disease severity and prognosis. Significant decrease of both natriuretic peptide and hypertrophy after left ventricular assist device (LVAD) treatment was reported. This study investigated whether chromogranin A and neural cell adhesion molecule (NCAM)/CD56 are associated with cardiac hypertrophy and regulated by LVAD. METHODS: Expression of atrial and brain natriuretic peptide, chromogranin A, and NCAM/CD56 were investigated by immunohistochemistry and morphometrically quantified in 33 paired myocardial samples before and after LVAD. In a different set of patients, chromogranin A was evaluated in the plasma. Cardiomyocyte colocalization of brain natriuretic peptide and chromogranin A was visualized by immunofluorescence doublestaining. RESULTS: Natriuretic peptide and chromogranin A protein expression is significantly decreased after LVAD (p < 0.05). NCAM/CD56 expression remains unaltered by unloading. In contrast with natriuretic peptide, chromogranin A and NCAM/CD56 expression is not correlated with cardiomyocyte diameters. Although increased compared with controls, no significant differences for chromogranin A plasma levels were found before and after LVAD. Sarcoplasmic colocalization of chromogranin A and brain natriuretic peptide is considerably decreased after LVAD. CONCLUSIONS: Neither chromogranin A nor CD56 is associated with cardiac hypertrophy. Chromogranin A is significantly decreased by ventricular support. Sarcoplasmic colocalization of brain natriuretic peptide and chromogranin A is diminished after unloading. However, owing to its low expression, the negative regulation of chromogranin A is not reflected by plasma levels and thus does not appear to be an appropriate biomarker of reverse cardiac remodeling after unloading. |
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Authors:
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Jeremias Wohlschlaeger; Moritz von Winterfeld; Hendrik Milting; Aly El Banayosy; Klaus Jürgen Schmitz; Atsushi Takeda; Nobuakira Takeda; Petra Azhari; Christof Schmid; Christian August; Kurt Werner Schmid; Hideo Andreas Baba |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation Volume: 27 ISSN: 1557-3117 ISO Abbreviation: J. Heart Lung Transplant. Publication Date: 2008 Apr |
Date Detail:
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Created Date: 2008-03-31 Completed Date: 2008-04-29 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9102703 Medline TA: J Heart Lung Transplant Country: United States |
Other Details:
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Languages: eng Pagination: 442-9 Citation Subset: IM |
Affiliation:
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Department of Pathology and Neuropathology, University Hospital Essen, University of Duisburg-Essen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Antigens, CD56 / metabolism Child Child, Preschool Chromogranin A / metabolism Chronic Disease Down-Regulation Female Heart Failure / metabolism, pathology, physiopathology*, surgery* Heart-Assist Devices* Humans Hypertrophy Male Middle Aged Myocardium / metabolism* Myocytes, Cardiac / pathology Natriuretic Peptide, Brain / metabolism* Neural Cell Adhesion Molecules / metabolism Sarcoplasmic Reticulum / metabolism Tissue Distribution Ventricular Remodeling* |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD56; 0/Chromogranin A; 0/Neural Cell Adhesion Molecules; 114471-18-0/Natriuretic Peptide, Brain |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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