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Glomerular Endothelial Cells Are Maintained by Vascular Endothelial Growth Factor in the Adult Kidney.
Author(s) -
Yasunori Kitamoto,
Motohiro Takeya,
Hiroshi Tokunaga,
Kimio Tomita
Publication year - 2001
Publication title -
tohoku journal of experimental medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.514
H-Index - 59
eISSN - 1349-3329
pISSN - 0040-8727
DOI - 10.1620/tjem.195.43
Subject(s) - glomerulus , vascular endothelial growth factor , kidney , biology , vascular endothelial growth factor b , endothelial stem cell , renal glomerulus , kidney glomerulus , vascular endothelial growth factor a , antibody , endocrinology , pathology , medicine , microbiology and biotechnology , glomerulonephritis , immunology , vegf receptors , cancer research , in vitro , biochemistry
Vascular endothelial growth factor (VEGF) is known to maintain endothelial cells of immature vessels and is constitutively expressed in the kidney from the embryo to adult. We tested the hypothesis that VEGF activity is needed to maintain glomerular endothelial cells in the adult. Neutralizing antibody to VEGF165 was intraperitoneally administered to mice for 3 days to strongly suppress its intrinsic activity. On the fourth day, mice were sacrificed and tissues were examined by light and electron microscopies. Vascular casts of renal vessels were observed by a scanning electron microscopy. Distribution of the administered antibody and expressions of VEGF and Flk-1 were examined immunohistochemically. The suppression of endogenous VEGF activity caused swelling and vacuolation of endothelial cells and obstruction of capillaries in the glomerulus. Other tissues were not impaired significantly. The administered antibody was specifically localized to the glomerulus, and was found more predominantly in the juxta-medullary than in the cortical glomerulus. This pattern of antibody deposition was similar to that of Flk-1. VEGF expression in the glomerulus was compensatively elevated by the antibody treatment. These results show that demand for VEGF signaling in the glomerulus is much higher than in other tissues, probably to protect its endothelial cells against high tension for blood filtration. This demand may be fulfilled by enriched signaling through the Flk-1 in the glomerulus.

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