The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Persistent eNOS activation secondary to caveolin-1 deficiency induces pulmonary hypertension in mice and humans through PKG nitration
Open accessAbstract
Pulmonary hypertension (PH) is an unremitting disease defined by a progressive increase in pulmonary vascular resistance leading to right-sided heart failure. Using mice with genetic deletions of caveolin 1 (Cav1) and eNOS (Nos3), we demonstrate here that chronic eNOS activation secondary to loss of caveolin-1 can lead to PH. Consistent with a role for eNOS in the pathogenesis of PH, the pulmonary vascular remodeling and PH phenotype of Cav1-/- mice were absent in Cav1-/-Nos3-/- mice. Further, treatment of Cav1-/- mice with either MnTMPyP (a superoxide scavenger) or l-NAME (a NOS inhibitor) reversed their pulmonary vascular pathology and PH phenotype. Activation of eNOS in Cav1-/- lungs led to the impairment of PKG activity through tyrosine nitration. Moreover, the PH phenotype in Cav1-/- lungs could be rescued by overexpression of PKG-1. The clinical relevance of the data was indicated by the observation that lung tissue from patients with idiopathic pulmonary arterial hypertension demonstrated increased eNOS activation and PKG nitration and reduced caveolin-1 expression. Together, these data show that loss of caveolin-1 leads to hyperactive eNOS and subsequent tyrosine nitration-dependent impairment of PKG activity, which results in PH. Thus, targeting of PKG nitration represents a potential novel therapeutic strategy for the treatment of PH.
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Beckman, J. S., Beckman, T. W., Chen, J., Marshall, P. A., & Freeman, B. A. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.4.1620 · Cited by 7,029
Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly
Beckman, J. S., & Koppenol, W. H. (1996) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.1996.271.5.c1424 · Cited by 5,513
Caveolin, a protein component of caveolae membrane coats
Rothberg, K. G., Heuser, J. E., Donzell, W. C., Ying, Y.-S., Glenney, J. R., & Anderson, R. G. W. (1992) · Cell · doi:10.1016/0092-8674(92)90143-z · Cited by 2,258
Protein S-nitrosylation: Purview and parameters
Hess, D. T., Matsumoto, A., Kim, S.-O., Marshall, H. E., & Stamler, J. S. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1569 · Cited by 2,153
Pulmonary Arterial Hypertension in France: Results from a National Registry
Humbert, M., Sitbon, O., Chaouat, A., Bertocchi, M., Habib, G., Gressin, V., Yaici, A., Weitzenblum, E., Cordier, J.-F., Chabot, F., et al. (2006) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200510-1668oc · Cited by 2,000
Expression of Endothelin-1 in the Lungs of Patients with Pulmonary Hypertension
Giaid, A., Yanagisawa, M., Langleben, D., Michel, R. P., Levy, R., Shennib, H., Kimura, S., Masaki, T., Duguid, W. P., & Stewart, D. J. (1993) · New England Journal of Medicine · doi:10.1056/nejm199306173282402 · Cited by 1,842
Primary Pulmonary Hypertension
Rubin, L. J. (1997) · New England Journal of Medicine · doi:10.1056/nejm199701093360207 · Cited by 1,726
Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice
Drab, M., Verkade, P., Elger, M., Kasper, M., Lohn, M., Lauterbach, B., Menne, J., Lindschau, C., Mende, F., Luft, F. C., et al. (2001) · Science · doi:10.1126/science.1062688 · Cited by 1,552
Lane, K. B., Machado, R. D., Pauciulo, M. W., Thomson, J. R., Phillips, J. A., Loyd, J. E., Nichols, W. C., & Trembath, R. C. (2000) · Nature Genetics · doi:10.1038/79226 · Cited by 1,495
Pulmonary Arterial Hypertension
Farber, H. W., & Loscalzo, J. (2004) · New England Journal of Medicine · doi:10.1056/nejmra035488 · Cited by 1,463
Cited by
Pulmonary Arterial Hypertension: The Clinical Syndrome
Lai, Y.-C., Potoka, K. C., Champion, H. C., Mora, A. L., & Gladwin, M. T. (2014) · Circulation Research · doi:10.1161/circresaha.115.301146 · Cited by 402
Endothelial cells in the pathogenesis of pulmonary arterial hypertension
Evans, C. E., Cober, N. D., Dai, Z., Stewart, D. J., & Zhao, Y.-Y. (2021) · European Respiratory Journal · doi:10.1183/13993003.03957-2020 · Cited by 325
Self-citationCaveolae, caveolins, and cavins: complex control of cellular signalling and inflammation
Chidlow, J. H., & Sessa, W. C. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq075 · Cited by 310
Safety of sapropterin dihydrochloride (6r–bh4) in patients with pulmonary hypertension
Robbins, I. M., Hemnes, A. R., Simon Gibbs, J., Christman, B. W., Howard, L., Meehan, S., Cabrita, I., Gonzalez, R., Oyler, T., Zhao, L., et al. (2011) · Experimental Lung Research · doi:10.3109/01902148.2010.512972 · Cited by 47
Therapeutics Targeting of Dysregulated Redox Equilibrium and Endothelial Dysfunction
Risbano, M. G., & Gladwin, M. T. (2013) · Handbook of Experimental Pharmacology · doi:10.1007/978-3-662-45805-1_13 · Cited by 32
Metadata
- Authors
- Zhao, Y.-Y., Zhao, Y. D., Mirza, M. K., Huang, J. H., Potula, H.-H. S. K., Vogel, S. M., Brovkovych, V., Yuan, J. X.-J., Wharton, J., & Malik, A. B.
- Venue
- Journal of Clinical Investigation
- Published
- 2009-07-01
- Volume
- 119
- Issue
- 7
- Pages
- 2009-2018
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2039879879
- Cited by
- 275
- References
- 57
- FWCI
- 16.01
- Type
- journal article
- Language
- en
- Open access
- green
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- Zhao, Y.-Y., Zhao, Y. D., Mirza, M. K., Huang, J. H., Potula, H.-H. S. K., Vogel, S. M., Brovkovych, V., Yuan, J. X.-J., Wharton, J., & Malik, A. B. (2009). Persistent eNOS activation secondary to caveolin-1 deficiency induces pulmonary hypertension in mice and humans through PKG nitration. Journal of Clinical Investigation. https://doi.org/10.1172/jci33338
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