No abstract

1 5 0 Supplement to Transplantation July 27, 2008, Volume 86 Number 2S remodeling, and the imbalance of collagenI (COLI) and collagen III (COL III). Losing the support of collagen, the function of left ventricular coverts from pressure pump to capacity, and eventually lead to heart failure. The CgA are released by sympathetic nerve terminals and counteract the actions of -adrenergic drugs. It is also showed that CgA can modulate fi broblast cell adhesion and spreading in a differential manner. So it is speculated that CgA could also contribute to regulate heart remodeling in patients with DCM. However, the correlation between CgA and myocardial fi brosis remained uncertain. In the present study, the expression and location of CgA and myocardial fi brosis in DCM were observed, so as to give rise to the further study in the role of the neuroendocrine of DCM and clinical evaluation of myocardial fi brosis. Methods; Surgical myocardial specimen from DCM patients, who were underwent successful orthotopic cardiac transplantation, and the normal myocardium were used for study objects. CgA, COLI and COL III expression were analyzed by RT-PCR. Location and expression of CgA were assessed by immunohistochemistry with anti-CgA antibody. The collagen specifi c picrosirus red staining was applied on slides of heart samples from controls and patients, and then the collagen volume fraction (CVF) was calculated. Results COLI-mRNA and COL III-mRNA were generated in all DCM patients, but not in the normal. CgA-mRNA was detected by RT-PCR in both normal and pathologic myocardium, while its expression was signifi cantly increased in DCM (P<0. 01). It is performed by immunohistochemistry that cytoplasic expression of CgA was showed in both normal and DCM paraffi n sections of myocardial samples. But a strong positive was produced in DCM slides (P<0. 01), densely arranged in the epicardial and endocardial myocardiocytes; while only few sparse granules were found in the normal. Increase of CVF and COLI deposition were obviously observed in DCM (P<0. 001). The deposition of COLI was surprisingly identical with the strong positive arrangement of CgA. Conclusions: It is demonstrated for the fi rst time that the deposition of CgA is related with the myocardial fi brosis of DCM, that is, CgA may infl uence the process of myocardial remodeling and fi brosis. CgA may represent a key player in nenuroendocrine regulation of DCM and it may be a potential diagnostic and prognostic indicators of DCM patients.