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Lack of endothelial diaphragms in fenestrae and caveolae of mutant Plvap-deficient mice


Boesl,  Michael R.
Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society;

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Herrnberger, L., Seitz, R., Kuespert, S., Boesl, M. R., Fuchshofer, R., & Tamm, E. R. (2012). Lack of endothelial diaphragms in fenestrae and caveolae of mutant Plvap-deficient mice. HISTOCHEMISTRY AND CELL BIOLOGY, 138(5), 709-724. doi:10.1007/s00418-012-0987-3.

Plasmalemmal vesicle-associated protein (PLVAP, PV-1) is specifically expressed in endothelial cells in which it localizes to diaphragms of fenestrae, caveolae, and transendothelial channels. To learn about its function, we generated mutant mice that lack PLVAP. In a C57BL/6N genetic background, homozygous Plvap-deficient embryos die before birth and suffer from subcutaneous edema, hemorrhages, and defects in the vascular wall of subcutaneous capillaries. In addition, hearts of Plvap (-/-) embryos show ventricular septal defects and thinner ventricular walls. In wild-type embryos, PLVAP and caveolae with a stomatal diaphragm are present in endothelial cells of subcutaneous capillaries and endocardium, while a diaphragm is missing in caveolae of Plvap (-/-) littermates. Plvap (-/-) mice in a mixed C57BL/6N/FVB-N genetic background are born and survive at the most for 4 weeks. Capillaries of exocrine and endocrine pancreas and of kidney peritubular interstitium were investigated in more detail as examples of fenestrated capillaries. In these vascular beds, Plvap (-/-) mice show a complete absence of diaphragms in fenestrae, caveolae, and transendothelial channels, findings which are associated with a substantial decrease in the number of endothelial fenestrae. The changes in the capillary phenotype correlate with a considerable retardation of postnatal growth and anemia. Plvap (-/-) mice provide an animal model to clarify the specific functional role of endothelial fenestrae and their contribution to passage of water and solutes in different organs.