The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Alterations in sarcoplasmic reticulum gene expression in human heart failure. A possible mechanism for alterations in systolic and diastolic properties of the failing myocardium.
Abstract
Recent studies have shown that intracellular Ca2+ handling is abnormal in the myocardium of patients with end-stage heart failure. Muscles from the failing hearts showed a prolonged Ca2+ transient and a diminished capacity to restore a low resting Ca2+ level during diastole. Accordingly, we examined whether this defect in Ca2+ transport function is due to alterations in sarcoplasmic reticulum gene expression. We determined the messenger RNA (mRNA) levels of sarcoplasmic reticulum Ca2+ transport proteins in failing human hearts from 17 cardiac transplant recipients with a diagnosis of dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The expression levels of each mRNA were compared with each other and then correlated with that of atrial natriuretic factor (ANF) mRNA in the failing ventricle. The mRNA levels for the calcium release channel (ryanodine receptor, RYR2), Ca2+ uptake pump (Ca(2+)-ATPase, SERCA2 isoform), and phospholamban differed significantly between heart samples but showed an inverse relation with that of ventricular ANF mRNA. In contrast, calsequestrin mRNA levels remained unchanged in these failing hearts. In addition, beta-myosin and alpha-cardiac actin mRNA levels also showed an inverse relation with ANF mRNA levels. These changes were observed in both right and left ventricles of hearts with congestive heart failure due to dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The results are consistent with the hypothesis that abnormal calcium handling in the sarcoplasmic reticulum of failing hearts is due to the altered expression of the genes encoding sarcoplasmic reticulum proteins.
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Cites
Primary structure and expression from complementary DNA of skeletal muscle ryanodine receptor
Takeshima, H., Nishimura, S., Matsumoto, T., Ishida, H., Kangawa, K., Minamino, N., Matsuo, H., Ueda, M., Hanaoka, M., Hirose, T., et al. (1989) · Nature · doi:10.1038/339439a0 · Cited by 1,146
Cited by
Jessup, M., Greenberg, B., Mancini, D., Cappola, T., Pauly, D. F., Jaski, B., Yaroshinsky, A., Zsebo, K. M., Dittrich, H., & Hajjar, R. J. (2011) · Circulation · doi:10.1161/circulationaha.111.022889 · Cited by 760
Alterations of Sarcoplasmic Reticulum Proteins in Failing Human Dilated Cardiomyopathy
Meyer, M., Schillinger, W., Pieske, B., Holubarsch, C., Heilmann, C., Posival, H., Kuwajima, G., Mikoshiba, K., Just, H., & Hasenfuss, G. (1995) · Circulation · doi:10.1161/01.cir.92.4.778 · Cited by 535
Jaski, B. E., Jessup, M. L., Mancini, D. M., Cappola, T. P., Pauly, D. F., Greenberg, B., Borow, K., Dittrich, H., Zsebo, K. M., & Hajjar, R. J. (2009) · Journal of Cardiac Failure · doi:10.1016/j.cardfail.2009.01.013 · Cited by 457
Arias, M. A., García-Río, F., Alonso-Fernández, A., Mediano, O., Martínez, I., & Villamor, J. (2005) · Circulation · doi:10.1161/circulationaha.104.501841 · Cited by 420
Pogwizd, S. M., Qi, M., Yuan, W., Samarel, A. M., & Bers, D. M. (1999) · Circulation Research · doi:10.1161/01.res.85.11.1009 · Cited by 399
Metadata
- Authors
- Arai, M., Alpert, N. R., MacLennan, D. H., Barton, P., & Periasamy, M.
- Venue
- Circulation Research
- Published
- 1993-02
- Volume
- 72
- Issue
- 2
- Pages
- 463-469
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2122991452
- Cited by
- 479
- References
- 1
- FWCI
- 23.03
- Type
- journal article
- Language
- en
- Open access
- closed
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- Arai, M., Alpert, N. R., MacLennan, D. H., Barton, P., & Periasamy, M. (1993). Alterations in sarcoplasmic reticulum gene expression in human heart failure. A possible mechanism for alterations in systolic and diastolic properties of the failing myocardium. Circulation Research. https://doi.org/10.1161/01.res.72.2.463
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