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Publication : Vascular abnormalities in mice lacking the endothelial gap junction proteins connexin37 and connexin40.

First Author  Simon AM Year  2002
Journal  Dev Biol Volume  251
Issue  2 Pages  206-20
PubMed ID  12435353 Mgi Jnum  J:80178
Mgi Id  MGI:2445243 Doi  10.1006/dbio.2002.0826
Citation  Simon AM, et al. (2002) Vascular Abnormalities in Mice Lacking the Endothelial Gap Junction Proteins connexin37 and connexin40. Dev Biol 251(2):206-20
abstractText  Cells within the vascular wall are coupled by gap junctions, allowing for direct intercellular transfer of low molecular weight molecules. Although gap junctions are believed to be important for vascular development and function, their precise roles are not well understood. Mice lacking either connexin37 (Cx37) or connexin40 (Cx40), the predominant gap junction proteins present in vascular endothelium, are viable and exhibit phenotypes that are largely non-blood vessel related. Since Cx37 and Cx40 are coexpressed in endothelial cells and could overlap functionally, some roles of junctional communication may only be revealed by the elimination of both connexins. In this study, we interbreed Cx37 and Cx40 knockout mice to generate Cx37(-/-)Cx40(-/-) animals and show that they display severe vascular abnormalities and die perinatally. Cx37(-/-)Cx40(-/-) animals exhibit localized hemorrhages in skin, testis, gastrointestinal tissues, and lungs, with pronounced blood vessel dilatation and congestion occurring in some areas. Vascular anomalies were particularly striking in testis and intestine. In testis, abnormal vascular channels were present, with these channels coalescing into a cavernous, endothelium-lined blood pool resembling a hemangioma. These results provide evidence of a critical role for endothelial gap junction-mediated communication in the development and/or functional maintenance of segments of the mouse vasculature.
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