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Immunohistochemical examination of renal neovascularization in ischemia
Author(s) -
Baderca Flavia,
Zahoi Delia Elena,
Daescu Ecaterina,
Alexa Aurora
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb51
Subject(s) - neovascularization , cd31 , angiogenesis , pathology , medicine , ischemia , immunohistochemistry , vascular endothelial growth factor , cd34 , biology , vegf receptors , stem cell , microbiology and biotechnology
Neovascularization represents an important physiological response in ischemia. Renal neovascularization was already demonstrated in hypercholesterolemia. Probably, the trigger was ischemia as result of renal vasoconstriction. Renal neovascularization in primitive stages of atherosclerosis could be determinate by inflammation, an important mediator of angiogenesis. The study was retrospective, using kidneys samples taken at autopsy from 56 patients. Sections were stained with haematoxylin‐eosin method and immunohistochemically for CD31, CD34 and VEGF. With endothelial antibodies, the neovascularization was demonstrated by the presence of newly formed endothelial tubes originated from the endothelial cells of the veins’ luminal surface. They seep through the venous wall, from intima to adventicial tissue. These vascular elements were localized at venous‐tubular interface, parallel to adjacent collector ducts. At the same level, all cases presented an intense immunoreaction for VEGF in the cells lining the collecting ducts. In conclusion, the source of renal neovascularization was represented in the most cases by the adventicial blood vessels, but in the presence of ischemia the new formed blood vessels originated from luminal endothelial cells. More, the site of neovascularization was correlated with the expression of VEGF.