- About this Journal ·
- Abstracting and Indexing ·
- Aims and Scope ·
- Annual Issues ·
- Article Processing Charges ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Recently Accepted Articles ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 686972, 9 pages
Oxidative Stress Contributes to Endothelial Dysfunction in Mouse Models of Hereditary Hemorrhagic Telangiectasia
1Molecular Structure and Function Program, Hospital for Sick Children, Toronto, ON, Canada M5G 1X8
2Heart and Stroke Richard Lewar Center of Excellence, University of Toronto, ON, Canada M5S 3E2
3Department of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8
Received 9 November 2012; Accepted 30 November 2012
Academic Editor: Sumitra Miriyala
Copyright © 2012 Mirjana Jerkic et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- J. McDonald, P. Bayrak-Toydemir, and R. E. Pyeritz, “Hereditary hemorrhagic telangiectasia: an overview of diagnosis, management, and pathogenesis,” Genetics in Medicine, vol. 13, no. 7, pp. 607–616, 2011.
- N. P. Barbara, J. L. Wrana, and M. Letarte, “Endoglin is an accessory protein that interacts with the signaling receptor complex of multiple members of the transforming growth factor-β superfamily,” Journal of Biological Chemistry, vol. 274, no. 2, pp. 584–594, 1999.
- L. David, C. Mallet, S. Mazerbourg, J. J. Feige, and S. Bailly, “Identification of BMP9 and BMP10 as functional activators of the orphan activin receptor-like kinase 1 (ALK1) in endothelial cells,” Blood, vol. 109, no. 5, pp. 1953–1961, 2007.
- C. J. Gallione, G. M. Repetto, E. Legius et al., “A combined syndrome of juvenile polyposis and hereditary haemorrhagic telangiectasia associated with mutations in MADH4 (SMAD4),” The Lancet, vol. 363, no. 9412, pp. 852–859, 2004.
- S. G. Cole, M. E. Begbie, G. M. F. Wallace, and C. L. L. Shovlin, “A new locus for hereditary haemorrhagic telangiectasia (HHT3) maps to chromosome 5,” Journal of Medical Genetics, vol. 42, no. 7, pp. 577–582, 2005.
- P. Bayrak-Toydemir, J. McDonald, N. Akarsu et al., “A fourth locus for hereditary hemorrhagic telangiectasia maps to chromosome 7,” American Journal of Medical Genetics A, vol. 140, no. 20, pp. 2155–2162, 2006.
- J. Berg, M. Porteous, D. Reinhardt et al., “Hereditary haemorrhagic telangiectasia: a questionnaire based study to delineate the different phenotypes caused by endoglin and ALK1 mutations,” Journal of Medical Genetics, vol. 40, no. 8, pp. 585–590, 2003.
- T. G. W. Letteboer, J. J. Mager, R. J. Snijder, et al., “Genotype-phenotype relation in hereditary hemorrhagic teleangiectasia,” Journal of Medical Genetics, vol. 43, no. 4, pp. 371–377, 2006.
- N. Pece-Barbara, U. Cymerman, S. Vera, D. A. Marchuk, and M. Letarte, “Expression analysis of four endoglin missense mutations suggests that haploinsufficiency is the predominant mechanism for hereditary hemorrhagic telangiectasia type 1,” Human Molecular Genetics, vol. 8, no. 12, pp. 2171–2181, 1999.
- N. Ricard, M. Bidart, C. Mallet et al., “Functional analysis of the BMP9 response of ALK1 mutants from HHT2 patients: a diagnostic tool for novel ACVRL1 mutations,” Blood, vol. 116, no. 9, pp. 1604–1612, 2010.
- A. Bourdeau, D. J. Dumont, and M. Letarte, “A murine model of hereditary hemorrhagic telangiectasia,” Journal of Clinical Investigation, vol. 104, no. 10, pp. 1343–1351, 1999.
- S. Srinivasan, M. A. Hanes, T. Dickens et al., “A mouse model for hereditary hemorrhagic telangiectasia (HHT) type 2,” Human Molecular Genetics, vol. 12, no. 5, pp. 473–482, 2003.
- M. Jerkic, J. V. Rivas-Elena, M. Prieto, et al., “Endoglin regulates nitric oxide-dependent vasodilatation,” The FASEB Journal, vol. 18, no. 3, pp. 609–611, 2004.
- M. Toporsian, R. Gros, M. G. Kabir et al., “A role for endoglin in coupling eNOS activity and regulating vascular tone revealed in hereditary hemorrhagic telangiectasia,” Circulation Research, vol. 96, no. 6, pp. 684–692, 2005.
- M. Toporsian, M. Jerkic, Y. Q. Zhou et al., “Spontaneous adult-onset pulmonary arterial hypertension attributable to increased endothelial oxidative stress in a murine model of hereditary hemorrhagic telangiectasia,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 30, no. 3, pp. 509–517, 2010.
- M. Jerkic, M. G. Kabir, A. Davies, et al., “Pulmonary hypertension in adult Alk1 heterozygous mice due to oxidative stress,” Cardiovascular Research, vol. 92, no. 3, pp. 375–384, 2011.
- A. C. Montezano and R. M. Touyz, “Reactive oxygen species and endothelial function - role of nitric oxide synthase uncoupling and Nox family nicotinamide adenine dinucleotide phosphate oxidases,” Basic and Clinical Pharmacology and Toxicology, vol. 110, no. 1, pp. 87–94, 2012.
- T. Seki, J. Yun, and S. P. Oh, “Arterial endothelium-specific activin receptor-like kinase 1 expression suggests its role in arterialization and vascular remodeling,” Circulation Research, vol. 93, no. 7, pp. 682–689, 2003.
- I. B. Copland, D. Reynaud, C. Pace-Asciak, and M. Post, “Mechanotransduction of stretch-induced prostanoid release by fetal lung epithelial cells,” American Journal of Physiology, vol. 291, no. 3, pp. L487–L495, 2006.
- T. Finkel, “Signal transduction by reactive oxygen species,” Journal of Cellular Biology, vol. 194, no. 1, pp. 7–15, 2011.
- G. Kojda and D. Harrison, “Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure,” Cardiovascular Research, vol. 43, no. 3, pp. 562–571, 1999.
- S. Dikalov, K. K. Griendling, and D. G. Harrison, “Measurement of reactive oxygen species in cardiovascular studies,” Hypertension, vol. 49, no. 4, pp. 717–727, 2007.
- S. A. Abdalla and M. Letarte, “Hereditary haemorrhagic telangiectasia: current views on genetics and mechanisms of disease,” Journal of Medical Genetics, vol. 43, no. 2, pp. 97–110, 2006.
- J. Belik, M. Jerkic, B. A. S. McIntyre et al., “Age-dependent endothelial nitric oxide synthase uncoupling in pulmonary arteries of endoglin heterozygous mice,” American Journal of Physiology, vol. 297, no. 6, pp. L1170–L1178, 2009.
- R. C. Trembath, J. R. Thomson, R. D. Machado, et al., “Clinical and molecular genetic features of pulmonary hypertension in patients with hereditary hemorrhagic telangiectasia,” The New England Journal of Medicine, vol. 345, no. 5, pp. 325–334, 2001.
- B. Girerd, D. Montani, F. Coulet et al., “Clinical outcomes of pulmonary arterial hypertension in patients carrying an ACVRL1 (ALK1) mutation,” American Journal of Respiratory and Critical Care Medicine, vol. 181, no. 8, pp. 851–861, 2010.
- C. J. Mache, A. Gamillscheg, H. H. Popper, and S. G. Haworth, “Early-life pulmonary arterial hypertension with subsequent development of diffuse pulmonary arteriovenous malformations in hereditary haemorrhagic telangiectasia type 1,” Thorax, vol. 63, no. 1, pp. 85–86, 2008.
- R. D. Machado, M. A. Aldred, V. James, et al., “Mutations of the TGF-b Type II receptor BMPR2 in pulmonary arterial hypertension,” Human Mutation, vol. 27, no. 2, pp. 121–132, 2006.
- J. L. Cracowski, C. Cracowski, G. Bessard et al., “Increased lipid peroxidation in patients with pulmonary hypertension,” American Journal of Respiratory and Critical Care Medicine, vol. 164, no. 6, pp. 1038–1042, 2001.
- R. Bowers, C. Cool, R. C. Murphy, et al., “Oxidative stress in severe pulmonary hypertension,” American Journal of Respiratory and Critical Care Medicine, vol. 169, no. 6, pp. 764–769, 2004.
- J. F. Santibanez, F. J. Blanco, E. M. Garrido-Martin, F. Sanz-Rodriguez, M. A. Del Pozo, and C. Bernabeu, “Caveolin-1 interacts and cooperates with the transforming growth factor-β type I receptor ALK1 in endothelial caveolae,” Cardiovascular Research, vol. 77, no. 4, pp. 791–799, 2008.
- J. F. Gielis, J. Y. Lin, K. Wingler, P. E. Y. Van Schil, H. H. Schmidt, and A. L. Moens, “Pathogenetic role of eNOS uncoupling in cardiopulmonary disorders,” Free Radical Biology and Medicine, vol. 50, no. 7, pp. 765–776, 2011.
- E. L. Bell, T. A. Klimova, J. Eisenbart et al., “The Qo site of the mitochondrial complex III is required for the transduction of hypoxic signaling via reactive oxygen species production,” Journal of Cell Biology, vol. 177, no. 6, pp. 1029–1036, 2007.
- F. Di Lisa, N. Kaludercic, A. Carpi, R. Menabò, and M. Giorgio, “Mitochondria and vascular pathology,” Pharmacological Reports, vol. 61, no. 1, pp. 123–130, 2009.
- B. Chance, H. Sies, and A. Boveris, “Hydroperoxide metabolism in mammalian organs,” Physiological Reviews, vol. 59, no. 3, pp. 527–605, 1979.
- Y. Li, T. T. Huang, E. J. Carlson et al., “Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase,” Nature Genetics, vol. 11, no. 4, pp. 376–381, 1995.
- J. R. Henderson, H. Swalwell, S. Boulton, P. Manning, C. J. McNeil, and M. A. Birch-Machin, “Direct, real-time monitoring of superoxide generation in isolated mitochondria,” Free Radical Research, vol. 43, no. 9, pp. 796–802, 2009.
- T. Wajima, S. Shimizu, T. Hiroi, M. Ishii, and Y. Kiuchi, “Reduction of myocardial infarct size by tetrahydrobiopterin: possible involvement of mitochondrial KATP channels activation through nitric oxide production,” Journal of Cardiovascular Pharmacology, vol. 47, no. 2, pp. 243–249, 2006.
- J. C. Chang, S. J. Kou, W. T. Lin, and C. S. Liu, “Regulatory role of mitochondria in oxidative stress and atherosclerosis,” World Journal of Cardiology, vol. 2, no. 6, pp. 150–159, 2010.
- R. S. Frey, M. Ushio-Fukai, and A. B. Malik, “NADPH oxidase-dependent signaling in endothelial cells: role in physiology and pathophysiology,” Antioxidants and Redox Signaling, vol. 11, no. 4, pp. 791–810, 2009.
- A. Schramm, P. Matusik, G. Osmenda, and T. J. Guzik, “Targeting NADPH oxidases in vascular pharmacology,” Vascular Pharmacology, vol. 56, no. 5-6, pp. 216–231, 2012.
- J. Feng, S. M. Damrauer, M. Lee, F. W. Sellke, C. Ferran, and M. R. Abid, “Endothelium-dependent coronary vasodilatation requires NADPH oxidase-derived reactive oxygen species,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 30, no. 9, pp. 1703–1710, 2010.
- S. Wind, K. Beuerlein, T. Eucker, et al., “Comparative pharmacology of chemically distinct NADPH oxidase inhibitors,” British Journal of Pharmacology, vol. 161, no. 4, pp. 885–898, 2010.
- E. M. De Gussem, R. J. Snijder, F. J. Disch, P. Zanen, C. J. J. Westermann, and J. J. Mager, “The effect of N-acetylcysteine on epistaxis and quality of life in patients with HHT: a pilot study,” Rhinology, vol. 47, no. 1, pp. 85–88, 2009.
- K. Sugamura and J. F. Keaney Jr., “Reactive oxygen species in cardiovascular disease,” Free Radical Biology and Medicine, vol. 51, no. 5, pp. 978–992, 2011.