NDLI: Endothelial cell-specific knockout of connexin 43 causes hypotension and bradycardia in mice.

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Endothelial cell-specific knockout of connexin 43 causes hypotension and bradycardia in mice.

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Endothelial cell-specific knockout of connexin 43 causes hypotension and bradycardia in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Damon, D. N. Liao, Y. Day, K. H. Duling, B. R.
Description	Author Affiliation: Liao Y ( Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville 22908-0736, USA.);
Abstract	Connexin 43 (Cx43) is a protein expressed in a variety of mammalian tissues. However, the lack of specific blockers and the absence of known genetic mutants have hampered the investigation of the function of this protein. Cx43-null mice die shortly after birth, thus preventing functional studies in vivo. Here, we report the generation and characterization of a vascular endothelial cell-specific deletion of the Cx43 gene (VEC Cx43 KO) in mice by using the loxP/Cre system. Using homologous recombination, a mouse line was created carrying loxP sites flanking exon 2 of the Cx43 gene ('floxed' mice). To produce cell specific deletion of the Cx43 gene, these mice were crossed with animals from a line carrying the Tie 2-Cre transgene. The homozygous VEC Cx43 KO mice survived to maturity. However, they were hypotensive and bradycardic when compared with heterozygous VEC Cx43 KO mice, or to the floxed Cx43 gene mice. The hypotension was associated with marked elevation of plasma nitric oxide (NO) levels as well as elevated plasma angiotensin (Ang) I and II. We hypothesize that endothelial cell Cx43 plays a key role in the formation and/or action of NO, and that the elevation of Ang II is a secondary event. The specific cellular basis for the hypotension remains to be established, but our findings support the idea that endothelial Cx43 gap junctions are involved in maintaining normal vascular function; moreover, these animals provide the opportunity to determine more clearly the role of endothelial Cx43 in vascular development and homeostasis.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bradycardia Genetics Connexin 43 Physiology Endothelium, Vascular Metabolism Gap Junctions Hypotension Integrases Receptor Protein-Tyrosine Kinases Viral Proteins Angiotensin I Blood Angiotensin II Animals Cell Communication Deficiency Physiopathology Exons Gene Deletion Gene Expression Regulation Genes, Synthetic Homeostasis Biosynthesis Mice Mice, Inbred C57BL Mice, Knockout Models, Animal Nitric Oxide Organ Specificity Promoter Regions, Genetic Receptor, TIE-2 Recombinant Fusion Proteins Recombination, Genetic Regulatory Sequences, Nucleic Acid Transgenes Vascular Resistance Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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