Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to elucidate changes in respiratory muscles and their mechanism in cardiomyopathy. The contractile properties and histology of the diaphragm, as well as serum levels of insulin-like growth factor (IGF)-1, were examined in 10 hamsters with idiopathic dilated cardiomyopathy (CM) and 10 controls. At 28 weeks, body weight in CM was reduced compared with controls (114+/-10 versus 144+/-14 g, p<0.0001). The ratio of diaphragm to body weight was significantly higher in CM than in controls (0.228+/-0.015 versus 0.182+/-0.017, p<0.0001). In vitro, maximal diaphragmatic twitch (303+/-63 versus 455+/-119 g x cm(-2)) and tetanic tensions (1,555+/-369 versus 2,204+/-506 g x cm(-2)) were significantly lower in CM than in controls (p<0.005). The half-relaxation time was significantly shorter in CM (19+/-1 ms) than in controls (24+/-3 ms, p<0.0005). Fatiguability at 25 Hz was significantly less in CM (28%) than in controls (42%, p<0.0001). Diaphragm and gastrocnemius adenosine triphosphatase staining showed type I fibre atrophy in CM, associated with an increase in the number of type I fibres in the diaphragm. Histological examination of both muscles revealed an abnormal muscular pattern. Finally, serum levels of IGF-1 were 47% lower in the CM group than in controls (p<0.0001) and were clearly related to the changes in the contractile properties and histology of the diaphragm. In conclusion, cardiomyopathy in hamsters: 1) depressed the force-generating capacity and shortened the relaxation of the hamster diaphragm; 2) induced type I fibre atrophy in combination with a myopathic pattern; and 3) was associated with a significant reduction in serum levels of insulin-like growth factor-1, related to the diaphragmatic changes. Whether these changes are primary myopathic or secondary to heart failure remains to be elucidated.
 ...
PMID:Effects of dilated cardiomyopathy on the diaphragm in the Syrian hamster. 1006 87

Many hearts in end-stage, chronic failure (CHF) retain the capacity to reverse abnormal expression of genes regulating myocyte calcium cycling when supported with a left ventricular assist device (LVAD). In the present study, we determined whether LVAD-induced upregulation of the gene encoding for the key calcium cycling protein sarcoplasmic endoreticular calcium adenosine triphosphatase subtype 2a (SERCA2a) is influenced by the nature of underlying disease broadly characterized as ischemic (ICM) or idiopathic dilated (DCM) cardiomyopathy. Data from Northern blot analysis of SERCA2a messenger (m)RNA within 84 heart samples (50 CHF [23 DCM and 27 ICM] and 34 CHF+LVAD [18 DCM and 16 ICM]) were used for characterizing gene expression. In addition, measurements of the force-frequency relationship (FFR), a reflection of in vivo SERCA2a function, were obtained in myocardial trabeculae isolated from 75 hearts (51 CHF [29 DCM and 22 ICM] and 24 CHF+LVAD [10 DCM and 14 ICM]). SERCA2a mRNA demonstrated upregulation after LVAD that was not influenced by ICM or DCM. However, only in DCM hearts was the proportion of trabeculae exhibiting a normal FFR increased after LVAD. Thus, although upregulated SERCA2a gene expression after LVAD support is independent of myopathic origin, normalization of myocardial FFR, an index of SERCA2a function, is not. These data provide new insight into the process of cardiac "reverse molecular remodeling," and underscore potential differences in the impact of disease processes on posttranscriptional events.
 ...
PMID:Cardiomyopathic etiology and SERCA2a reverse remodeling during mechanical support of the failing human heart. 1636 1