Elevated blood pressure and craniofacial abnormalities in mice deficient in endothelin-1.

Abstract

The endothelin-1 (ET-1) gene was disrupted in mouse embryonic stem cells by homologous recombination to generate mice deficient in ET-1. These ET-1-/- homozygous mice die of respiratory failure at birth and have morphological abnormalities of the pharyngeal-arch-derived craniofacial tissues and organs. ET-1+/- heterozygous mice, which produce lower levels of ET-1 than wild-type mice, develop elevated blood pressure. These results suggest that ET-1 is essential for normal mouse development and may also play a physiological role in cardiovascular homeostasis.

• Authors: Y Kurihara, H Kurihara, H Suzuki, T Kodama, K Maemura, R Nagai, H Oda, T Kuwaki, W H Cao, N Kamada
• Journal: Nature (Nature) Vol. 368 Issue 6473 Pg. 703-10 (Apr 21 1994) ISSN: 0028-0836 [Print] England
• PMID: 8152482 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• DNA Primers
• Endothelins

Topics

• Animals
• Base Sequence
• Blood Pressure (genetics, physiology)
• Branchial Region (abnormalities, embryology)
• DNA Primers
• Embryonic and Fetal Development (genetics)
• Endothelins (deficiency, genetics, physiology)
• Female
• Heterozygote
• Homozygote
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Inbred ICR
• Molecular Sequence Data
• Organ Culture Techniques
• Respiratory Insufficiency (genetics)
• Skull (abnormalities)
• Stem Cells