کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3146302 1197209 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Receptor for advanced glycation end products (RAGE)-expressing endothelial cells co-express AGE and S100 in human periapical granulomas
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی دندانپزشکی، جراحی دهان و پزشکی
پیش نمایش صفحه اول مقاله
Receptor for advanced glycation end products (RAGE)-expressing endothelial cells co-express AGE and S100 in human periapical granulomas
چکیده انگلیسی

ObjectiveThe engagement of the receptor for advanced glycation end products (RAGE) by AGE or S100 perturbs homeostatic mechanisms and provides a basis for cellular dysfunction in pathological situations. To assess the mechanism of vascular immune reactions in chronic periapical periodontitis, we analysed co-expression of RAGE and AGE or S100 in periapical granulomas.MethodsSurgically removed periapical lesions, which had been diagnosed as chronic periodontitis, were inspected histologically using paraffin-embedded sections stained with haematoxylin and eosin. Cryostat sections of the tissues, which were identified histologically as periapical granulomas, were then examined by double immunohistochemistry using polyclonal antibodies raised against human CD34 and monoclonal antibodies specific for human RAGE, AGE or S100. Dual-colour immunofluorescence image analysis was also performed to assess the co-expression of RAGE and AGE or RAGE and S100 by endothelial cells.ResultsMarked expression of RAGE, AGE, and S100 by CD34+ endothelial cells was noted. Dual-colour immunofluorescence image analysis revealed that the RAGE-expressing endothelial cells co-expressed AGE and S100; however, the number of RAGE–AGE-expressing endothelial cells was significantly higher than that of RAGE–S100-expressing endothelial cells.ConclusionsCo-expression of RAGE and AGE by endothelial cells in periapical granulomas is more relevant than that of RAGE and S100. The possible engagement of RAGE and AGE may trigger cellular activation and mediate tissue injury.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Dentistry - Volume 39, Issue 10, October 2011, Pages 679–685
نویسندگان
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