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Disruption of ECE-1 and ECE-2 reveals a role for endothelin-converting enzyme-2 in murine cardiac development
Open accessAbstract
Endothelin-converting enzyme-1 and -2 (ECE-1 and -2) are membrane-bound metalloproteases that can cleave biologically the inactive endothelin-1 (ET-1) precursor to form active ET-1 in vitro. We previously reported developmental defects in specific subsets of neural crest-derived tissues, including branchial arch-derived craniofacial structures, aortic arch arteries, and the cardiac outflow tract in ECE-1 knockout mice. To examine the role of ECE-2 in cardiovascular development, we have now generated a null mutation in ECE-2 by homologous recombination. ECE-2 null mice develop normally, are healthy into adulthood, are fertile in both sexes, and live a normal life span. However, when they are bred into an ECE-1-null background, defects in cardiac outflow structures become more severe than those in ECE-1 single knockout embryos. In addition, ECE-1(-/-); ECE-2(-/-) double null embryos exhibited abnormal atrioventricular valve formation, a phenotype never seen in ECE-1 single knockout embryos. In the developing mouse heart, ECE-2 mRNA is expressed in the endocardial cushion mesenchyme from embyronic day (E) 12.5, in contrast to the endocardial expression of ECE-1. Levels of mature ET-1 and ET-2 in whole ECE-1(-/-); ECE-2(-/-) embryos at E12.5 do not differ appreciably from those of ECE-1(-/-) embryos. The significant residual ET-1/ET-2 in the ECE-1(-/-); ECE-2(-/-) embryos indicates that proteases distinct from ECE-1 and ECE-2 can carry out ET-1 activation in vivo.
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Brannan, C. I., Perkins, A. S., Vogel, K. S., Ratner, N., Nordlund, M. L., Reid, S. W., Buchberg, A. M., Jenkins, N. A., Parada, L. F., & Copeland, N. G. (1994) · Genes & Development · doi:10.1101/gad.8.9.1019 · Cited by 641
Cited by
Davenport, A. P., Hyndman, K. A., Dhaun, N., Southan, C., Kohan, D. E., Pollock, J. S., Pollock, D. M., Webb, D. J., & Maguire, J. J. (2016) · Pharmacological Reviews · doi:10.1124/pr.115.011833 · Cited by 772
Brutsaert, D. L. (2003) · Physiological Reviews · doi:10.1152/physrev.00017.2002 · Cited by 697
Amiri, F., Virdis, A., Neves, M. F., Iglarz, M., Seidah, N. G., Touyz, R. M., Reudelhuber, T. L., & Schiffrin, E. L. (2004) · Circulation · doi:10.1161/01.cir.0000144462.08345.b9 · Cited by 346
Eckman, E. A., Adams, S. K., Troendle, F. J., Stodola, B. A., Kahn, M. A., Fauq, A. H., Xiao, H. D., Bernstein, K. E., & Eckman, C. B. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m605827200 · Cited by 196
Metadata
- Authors
- Yanagisawa, H., Hammer, R. E., Richardson, J. A., Emoto, N., Williams, S. C., Takeda, S.-I., Clouthier, D. E., & Yanagisawa, M.
- Venue
- Journal of Clinical Investigation
- Published
- 2000-05-15
- Volume
- 105
- Issue
- 10
- Pages
- 1373-1382
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1985592940
- Cited by
- 190
- References
- 1
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- green
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- Yanagisawa, H., Hammer, R. E., Richardson, J. A., Emoto, N., Williams, S. C., Takeda, S.-I., Clouthier, D. E., & Yanagisawa, M. (2000). Disruption of ECE-1 and ECE-2 reveals a role for endothelin-converting enzyme-2 in murine cardiac development. Journal of Clinical Investigation. https://doi.org/10.1172/jci7447
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