{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T15:45:30Z","timestamp":1760888730351},"reference-count":50,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,9,7]],"date-time":"2012-09-07T00:00:00Z","timestamp":1346976000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>The aim of the present study was to investigate the possible microvascular regulatory role of vascular endothelial growth factor receptor type 2 (<jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2) in experimental gingivitis in rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Background<\/jats:title><jats:p>Our previous results demonstrated that functionally active <jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2s are located in the venules of rat gingiva. While there is no remarkable endogenous gingival <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> production under normal circumstances, exogenous <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>, via <jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2, shows venodilatory effects. We assumed that <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis) of gingival inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Gingivitis was induced by placing ligatures and composite material around and between the lower incisors of anesthetized Wistar rats next to the gingival margin. Seven days later, <jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2 antagonist (<jats:styled-content style=\"fixed-case\">ZM<\/jats:styled-content>323881), was dripped upon the labial gingiva next to the lower incisors. Diameter changes of the selected gingival venules were measured by vital microscopy. Animals with healthy gingiva served as controls. Venule diameter changes were compared to the baseline and to control groups (no ligature). Immunohistochemical and Western blot analysis for <jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2 were utilized.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>After 15, 30 and 60\u00a0min of local application of <jats:styled-content style=\"fixed-case\">ZM<\/jats:styled-content>323881, there was a significant venoconstriction in the inflamed gingiva compared to the baseline, while no change was recorded in controls. Endothelium, smooth muscle cells and pericytes of the gingivitis group showed increased <jats:styled-content style=\"fixed-case\">VEGFR<\/jats:styled-content>2 expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings suggest that there is an increased <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> production in gingivitis, which may play an important role in vasodilation of rat gingival venules.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1600-0765.2012.01520.x","type":"journal-article","created":{"date-parts":[[2012,9,7]],"date-time":"2012-09-07T13:29:54Z","timestamp":1347024594000},"page":"194-202","source":"Crossref","is-referenced-by-count":3,"title":["Microvascular regulatory role and increased expression of vascular endothelial growth factor receptor type 2 in experimental gingivitis"],"prefix":"10.1111","volume":"48","author":[{"given":"M.","family":"Gyurkovics","sequence":"first","affiliation":[{"name":"Department of Conservative Dentistry, Faculty of Dentistry Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Z.","family":"Lohinai","sequence":"additional","affiliation":[{"name":"Department of Conservative Dentistry, Faculty of Dentistry Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Gy\u0151rfi","sequence":"additional","affiliation":[{"name":"Department of Conservative Dentistry, Faculty of Dentistry Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Bodor","sequence":"additional","affiliation":[{"name":"Institute of Pathophysiology, Faculty of Medicine Hungarian Academy of Sciences and Semmelweis University Research Group for Pediatrics and Nephrology, Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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