| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Brief Communication
1 Center for Molecular Genetics, Department of Molecular Cardiology, Cleveland Clinic Foundation, Cleveland 44195
2 Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland 44195
3 Department of Biology, Cleveland State University, Cleveland 44115
4 Kaufman Center for Heart Failure, Department of Cardiovascular Medicine, Cleveland, Ohio 44195
5 Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, Ohio 44195
Coronary artery disease (CAD) is the leading cause of mortality and morbidity in developed nations. We hypothesized that CAD is associated with distinct patterns of protein expression in the coronary arteries, and we have begun to employ proteomics to identify differentially expressed proteins in diseased coronary arteries. Two-dimensional (2-D) gel electrophoresis of proteins and subsequent mass spectrometric analysis identified the ferritin light chain as differentially expressed between 10 coronary arteries from patients with CAD and 7 coronary arteries from normal individuals. Western blot analysis indicated significantly increased expression of the ferritin light chain in the diseased coronary arteries (1.41 vs. 0.75; P = 0.01). Quantitative real-time PCR analysis showed that expression of ferritin light chain mRNA was decreased in diseased tissues (0.70 vs. 1.17; P = 0.013), suggesting that increased expression of ferritin light chain in CAD coronary arteries may be related to increased protein stability or upregulation of expression at the posttranscriptional level in the diseased tissues. Ferritin light chain protein mediates storage of iron in cells. We speculate that increased expression of the ferritin light chain may contribute to pathogenesis of CAD by modulating oxidation of lipids within the vessel wall through the generation of reactive oxygen species. Our results provide in situ proteomic evidence consistent with the "iron hypothesis," which proposes an association between excessive iron storage and a high risk of CAD. However, it is also possible that the increased ferritin expression in diseased coronary arteries is a consequence, rather than a cause, of CAD.
coronary artery disease; sudden death; atherosclerosis; proteomics
This article has been cited by other articles:
|
|
 |
|
  A. Zarjou, V. Jeney, P. Arosio, M. Poli, P. Antal-Szalmas, A. Agarwal, G. Balla, and J. Balla Ferritin Prevents Calcification and Osteoblastic Differentiation of Vascular Smooth Muscle Cells J. Am. Soc. Nephrol., June 1, 2009; 20(6): 1254 - 1263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Liao, Z. Liu, J. Bao, Z. Zhao, J. Hu, X. Feng, R. Feng, Q. Lu, Z. Mei, Y. Liu, et al. A proteomic study of the aortic media in human thoracic aortic dissection: Implication for oxidative stress J. Thorac. Cardiovasc. Surg., July 1, 2008; 136(1): 65 - 72. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Smith, E. C. Smith, M. L. Gilman, J. L. Anderson, and R. L. Taylor Jr. Differentially Expressed Soluble Proteins in Aortic Cells from Atherosclerosis-Susceptible and Resistant Pigeons Poult. Sci., July 1, 2008; 87(7): 1328 - 1334. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. U. Zimmerli, E. Schiffer, P. Zurbig, D. M. Good, M. Kellmann, L. Mouls, A. R. Pitt, J. J. Coon, R. E. Schmieder, K. H. Peter, et al. Urinary Proteomic Biomarkers in Coronary Artery Disease Mol. Cell. Proteomics, February 1, 2008; 7(2): 290 - 298. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. B. Hu The Iron-Heart Hypothesis: Search for the Ironclad Evidence JAMA, February 14, 2007; 297(6): 639 - 641. [Full Text] [PDF]
|
|
|
|
|
|
M. Mayr, J. Zhang, A. S. Greene, D. Gutterman, J. Perloff, and P. Ping Proteomics-based Development of Biomarkers in Cardiovascular Disease: Mechanistic, Clinical, and Therapeutic Insights Mol. Cell. Proteomics, October 1, 2006; 5(10): 1853 - 1864. [Full Text] [PDF]
|
|
|
|
 |
|
 L. M. Blanco-Colio, J. L. Martin-Ventura, F. Vivanco, J.-B. Michel, O. Meilhac, and J. Egido Biology of atherosclerotic plaques: What we are learning from proteomic analysis Cardiovasc Res, October 1, 2006; 72(1): 18 - 29. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Sloane, R. A. Lindner, S. S. Prasad, L. T. Sebastian, S. K. Pedersen, M. Robinson, P. T. Bye, D. W. Nielson, and J. L. Harry Proteomic Analysis of Sputum from Adults and Children with Cystic Fibrosis and from Control Subjects Am. J. Respir. Crit. Care Med., December 1, 2005; 172(11): 1416 - 1426. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Goralska, S. Nagar, L. N. Fleisher, and M. C. McGahan Differential Degradation of Ferritin H- and L-Chains: Accumulation of L-Chain-Rich Ferritin in Lens Epithelial Cells Invest. Ophthalmol. Vis. Sci., October 1, 2005; 46(10): 3521 - 3529. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. McRedmond, S. D. Park, D. F. Reilly, J. A. Coppinger, P. B. Maguire, D. C. Shields, and D. J. Fitzgerald Integration of Proteomics and Genomics in Platelets: A PROFILE OF PLATELET PROTEINS AND PLATELET-SPECIFIC GENES Mol. Cell. Proteomics, February 1, 2004; 3(2): 133 - 144. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. R. Archacki, G. Angheloiu, X.-L. Tian, F. L. Tan, N. DiPaola, G.-Q. Shen, C. Moravec, S. Ellis, E. J. Topol, and Q. Wang Identification of new genes differentially expressed in coronary artery disease by expression profiling Physiol Genomics, September 29, 2003; 15(1): 65 - 74. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
