The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Increased Expression of Cytoskeletal, Linkage, and Extracellular Proteins in Failing Human Myocardium
Abstract
Abstract —Experimental studies have shown that in hypertrophy and heart failure, accumulation of microtubules occurs that impedes sarcomere motion and contributes to decreased ventricular compliance. We tested the hypothesis that these changes are present in the failing human heart and that an entire complex of structural components, including cytoskeletal, linkage, and extracellular proteins, are involved in causing functional deterioration. In explanted human hearts failing because of dilated cardiomyopathy (ejection fraction ≤20%), expression of α- and β-tubulin, desmin, vinculin, fibronectin, and vimentin was determined by Northern and Western blot analysis and compared with normal myocardium from explants not used for transplantation. The mRNA for α- and β-tubulin was increased to 2.4-fold ( P <0.01) and 1.25-fold (NS), respectively; for desmin, 1.2-fold ( P <0.05); for fibronectin, 5-fold ( P <0.001); and for vimentin, 1.7-fold ( P <0.05). Protein levels for α-tubulin increased 2.6-fold ( P <0.02); for β-tubulin, 1.2-fold ( P <0.005); for desmin, 2.1-fold ( P <0.001); for vinculin, 1.2-fold ( P <0.005); for fibronectin, 2.9-fold ( P <0.001); and for vimentin, 1.5-fold ( P <0.005). Confocal microscopy showed augmentation and disorganization of all proteins studied. In combination with the loss of myofilaments and sarcomeric skeleton previously reported, these changes suggest cardiomyocyte remodeling. Increased fibronectin and elevated interstitial cellularity (vimentin labeling) indicate progressive fibrosis. The present results suggest a causative role of cytoskeletal abnormalities and myofilament loss for intrinsic contractile and diastolic dysfunction in failing hearts.
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Cites
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Cited by
Flett, A. S., Hayward, M. P., Ashworth, M. T., Hansen, M. S., Taylor, A. M., Elliott, P. M., McGregor, C., & Moon, J. C. (2010) · Circulation · doi:10.1161/circulationaha.109.930636 · Cited by 915
Myocytes Die by Multiple Mechanisms in Failing Human Hearts
Kostin, S., Pool, L., Elsässer, A., Hein, S., Drexler, H. C. A., Arnon, E., Hayakawa, Y., Zimmermann, R., Bauer, E., Klövekorn, W.-P., et al. (2003) · Circulation Research · doi:10.1161/01.res.0000067471.95890.5c · Cited by 564
Self-citationRoss, R. S., & Borg, T. K. (2001) · Circulation Research · doi:10.1161/hh1101.091862 · Cited by 451
Makarenko, I., Opitz, C. A., Leake, M. C., Neagoe, C., Kulke, M., Gwathmey, J. K., del Monte, F., Hajjar, R. J., & Linke, W. A. (2004) · Circulation Research · doi:10.1161/01.res.0000143901.37063.2f · Cited by 332
Enhanced autophagy ameliorates cardiac proteinopathy
Bhuiyan, M. S., Pattison, J. S., Osinska, H., James, J., Gulick, J., McLendon, P. M., Hill, J. A., Sadoshima, J., & Robbins, J. (2013) · Journal of Clinical Investigation · doi:10.1172/jci70877 · Cited by 298
Metadata
- Authors
- Heling, A., Zimmermann, R., Kostin, S., Maeno, Y., Hein, S., Devaux, B., Bauer, E., Klövekorn, W.-P., Schlepper, M., Schaper, W., & Schaper, J.
- Venue
- Circulation Research
- Published
- 2000-04-28
- Volume
- 86
- Issue
- 8
- Pages
- 846-853
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2098787491
- Cited by
- 326
- References
- 38
- FWCI
- 9.40
- Type
- journal article
- Language
- en
- Open access
- closed
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- Heling, A., Zimmermann, R., Kostin, S., Maeno, Y., Hein, S., Devaux, B., Bauer, E., Klövekorn, W.-P., Schlepper, M., Schaper, W., & Schaper, J. (2000). Increased Expression of Cytoskeletal, Linkage, and Extracellular Proteins in Failing Human Myocardium. Circulation Research. https://doi.org/10.1161/01.res.86.8.846
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