The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances

Zs. Lohinai, M. Gyurkovics, A. Gyorfi, C. Bodor, A. Székely, E. Dinya, L. Rosivall

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Background:. The VEGF is known to have endothelium derived effects through its type-2 receptor (VEGFR2), e.g. vascular permeability increase, regulation of endothelial cell proliferation, angiogenesis, etc. Nevertheless, there are only limited information about its role in the regulation of gingival microcirculation, especially in case of gingival venules. Aim: The main goal of our investigation was to evaluate the possible regulatory role of VEGF on the gingival venules of rats in physiological (healthy gingiva) and pathological (gingivitis) states. Material and Methods: Adult male Wistar rats were randomly divided into two experimental model groups: 1.) healthy gingiva, 2.) experimental gingivitis. Some rats of the first group were premedicated with nitric oxide (NO) synthesis blocker in drinking water for one week before the experiment. Animals of the gingivitis group received pretreatment in form of ligature around the lower incisors for 1 week. The investigated materials (VEGF, selective VEGFR2 antagonist, saline) were dripped onto the gingiva between the lower incisors. Vital microscopy combined with digital photography was used to observe the diameter changes of selected gingival venule at lower incisors in specified times. Venule diameter changes were compared to the start-up and to the values of the control group as well. Immunohistochemistry and western blot were also utilized to localize and to analyze VEGFR2s. Results: In healthy gingiva, VEGF significantly and dose-dependently increased the venule diameter compared to saline. VEGFR2 antagonist on its own did not cause any alteration. Premedication with the antagonist or NO synthase blocker decreased the dilatory effect of VEGF significantly. However, in case of gingivitis significant venoconstriction occured for the VEGFR2 antagonist. Furthermore, VEGFR2 overexpressions were also detected both with immunohistochemical and western blot analysis. It is worth emphasizing that in gingivitis all components and neighboring cells of the vessel wall express conspicuously higher amount of VEGFR2. Conclusion: Our results demonstrate that functionally active VEGFR2s are located in the venules of rat healthy gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2 activation and consequent endothelium derived NO release pathway, shows venodilatory effects. Furthermore, both VEGF production and VEGFR2 expressions are increased in gingiva during gingivitis. We assume that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis and remodeling of the local microvascular network) of gingiva in inflammation. Inhibition of VEGFR2s may be a new therapeutic approach of periodontal disease.

Original languageEnglish
Title of host publicationVascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance
PublisherNova Science Publishers, Inc.
Pages153-167
Number of pages15
ISBN (Print)9781626186552
Publication statusPublished - 2013

Fingerprint

Venules
Vascular Endothelial Growth Factor A
Gingiva
Gingivitis
Rats
Incisor
Nitric Oxide
Western Blotting
Microcirculation
Premedication
Photography
Endothelial cells
Cell proliferation
Capillary Permeability
Periodontal Diseases
Microvessels
Vasodilation
Nitric Oxide Synthase
Drinking Water
Cell Wall

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Lohinai, Z., Gyurkovics, M., Gyorfi, A., Bodor, C., Székely, A., Dinya, E., & Rosivall, L. (2013). The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances. In Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance (pp. 153-167). Nova Science Publishers, Inc..

The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances. / Lohinai, Zs.; Gyurkovics, M.; Gyorfi, A.; Bodor, C.; Székely, A.; Dinya, E.; Rosivall, L.

Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance. Nova Science Publishers, Inc., 2013. p. 153-167.

Research output: Chapter in Book/Report/Conference proceedingChapter

Lohinai, Z, Gyurkovics, M, Gyorfi, A, Bodor, C, Székely, A, Dinya, E & Rosivall, L 2013, The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances. in Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance. Nova Science Publishers, Inc., pp. 153-167.
Lohinai Z, Gyurkovics M, Gyorfi A, Bodor C, Székely A, Dinya E et al. The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances. In Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance. Nova Science Publishers, Inc. 2013. p. 153-167
Lohinai, Zs. ; Gyurkovics, M. ; Gyorfi, A. ; Bodor, C. ; Székely, A. ; Dinya, E. ; Rosivall, L. / The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances. Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance. Nova Science Publishers, Inc., 2013. pp. 153-167
@inbook{0ccdca4b83fa49f88e222f5bbb652f9e,
title = "The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances",
abstract = "Background:. The VEGF is known to have endothelium derived effects through its type-2 receptor (VEGFR2), e.g. vascular permeability increase, regulation of endothelial cell proliferation, angiogenesis, etc. Nevertheless, there are only limited information about its role in the regulation of gingival microcirculation, especially in case of gingival venules. Aim: The main goal of our investigation was to evaluate the possible regulatory role of VEGF on the gingival venules of rats in physiological (healthy gingiva) and pathological (gingivitis) states. Material and Methods: Adult male Wistar rats were randomly divided into two experimental model groups: 1.) healthy gingiva, 2.) experimental gingivitis. Some rats of the first group were premedicated with nitric oxide (NO) synthesis blocker in drinking water for one week before the experiment. Animals of the gingivitis group received pretreatment in form of ligature around the lower incisors for 1 week. The investigated materials (VEGF, selective VEGFR2 antagonist, saline) were dripped onto the gingiva between the lower incisors. Vital microscopy combined with digital photography was used to observe the diameter changes of selected gingival venule at lower incisors in specified times. Venule diameter changes were compared to the start-up and to the values of the control group as well. Immunohistochemistry and western blot were also utilized to localize and to analyze VEGFR2s. Results: In healthy gingiva, VEGF significantly and dose-dependently increased the venule diameter compared to saline. VEGFR2 antagonist on its own did not cause any alteration. Premedication with the antagonist or NO synthase blocker decreased the dilatory effect of VEGF significantly. However, in case of gingivitis significant venoconstriction occured for the VEGFR2 antagonist. Furthermore, VEGFR2 overexpressions were also detected both with immunohistochemical and western blot analysis. It is worth emphasizing that in gingivitis all components and neighboring cells of the vessel wall express conspicuously higher amount of VEGFR2. Conclusion: Our results demonstrate that functionally active VEGFR2s are located in the venules of rat healthy gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2 activation and consequent endothelium derived NO release pathway, shows venodilatory effects. Furthermore, both VEGF production and VEGFR2 expressions are increased in gingiva during gingivitis. We assume that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis and remodeling of the local microvascular network) of gingiva in inflammation. Inhibition of VEGFR2s may be a new therapeutic approach of periodontal disease.",
author = "Zs. Lohinai and M. Gyurkovics and A. Gyorfi and C. Bodor and A. Sz{\'e}kely and E. Dinya and L. Rosivall",
year = "2013",
language = "English",
isbn = "9781626186552",
pages = "153--167",
booktitle = "Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance",
publisher = "Nova Science Publishers, Inc.",

}

TY - CHAP

T1 - The role of vascular endothelial growth factor (VEGF) in the regulation of gingival venule diameter under physiological and pathological circumstances

AU - Lohinai, Zs.

AU - Gyurkovics, M.

AU - Gyorfi, A.

AU - Bodor, C.

AU - Székely, A.

AU - Dinya, E.

AU - Rosivall, L.

PY - 2013

Y1 - 2013

N2 - Background:. The VEGF is known to have endothelium derived effects through its type-2 receptor (VEGFR2), e.g. vascular permeability increase, regulation of endothelial cell proliferation, angiogenesis, etc. Nevertheless, there are only limited information about its role in the regulation of gingival microcirculation, especially in case of gingival venules. Aim: The main goal of our investigation was to evaluate the possible regulatory role of VEGF on the gingival venules of rats in physiological (healthy gingiva) and pathological (gingivitis) states. Material and Methods: Adult male Wistar rats were randomly divided into two experimental model groups: 1.) healthy gingiva, 2.) experimental gingivitis. Some rats of the first group were premedicated with nitric oxide (NO) synthesis blocker in drinking water for one week before the experiment. Animals of the gingivitis group received pretreatment in form of ligature around the lower incisors for 1 week. The investigated materials (VEGF, selective VEGFR2 antagonist, saline) were dripped onto the gingiva between the lower incisors. Vital microscopy combined with digital photography was used to observe the diameter changes of selected gingival venule at lower incisors in specified times. Venule diameter changes were compared to the start-up and to the values of the control group as well. Immunohistochemistry and western blot were also utilized to localize and to analyze VEGFR2s. Results: In healthy gingiva, VEGF significantly and dose-dependently increased the venule diameter compared to saline. VEGFR2 antagonist on its own did not cause any alteration. Premedication with the antagonist or NO synthase blocker decreased the dilatory effect of VEGF significantly. However, in case of gingivitis significant venoconstriction occured for the VEGFR2 antagonist. Furthermore, VEGFR2 overexpressions were also detected both with immunohistochemical and western blot analysis. It is worth emphasizing that in gingivitis all components and neighboring cells of the vessel wall express conspicuously higher amount of VEGFR2. Conclusion: Our results demonstrate that functionally active VEGFR2s are located in the venules of rat healthy gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2 activation and consequent endothelium derived NO release pathway, shows venodilatory effects. Furthermore, both VEGF production and VEGFR2 expressions are increased in gingiva during gingivitis. We assume that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis and remodeling of the local microvascular network) of gingiva in inflammation. Inhibition of VEGFR2s may be a new therapeutic approach of periodontal disease.

AB - Background:. The VEGF is known to have endothelium derived effects through its type-2 receptor (VEGFR2), e.g. vascular permeability increase, regulation of endothelial cell proliferation, angiogenesis, etc. Nevertheless, there are only limited information about its role in the regulation of gingival microcirculation, especially in case of gingival venules. Aim: The main goal of our investigation was to evaluate the possible regulatory role of VEGF on the gingival venules of rats in physiological (healthy gingiva) and pathological (gingivitis) states. Material and Methods: Adult male Wistar rats were randomly divided into two experimental model groups: 1.) healthy gingiva, 2.) experimental gingivitis. Some rats of the first group were premedicated with nitric oxide (NO) synthesis blocker in drinking water for one week before the experiment. Animals of the gingivitis group received pretreatment in form of ligature around the lower incisors for 1 week. The investigated materials (VEGF, selective VEGFR2 antagonist, saline) were dripped onto the gingiva between the lower incisors. Vital microscopy combined with digital photography was used to observe the diameter changes of selected gingival venule at lower incisors in specified times. Venule diameter changes were compared to the start-up and to the values of the control group as well. Immunohistochemistry and western blot were also utilized to localize and to analyze VEGFR2s. Results: In healthy gingiva, VEGF significantly and dose-dependently increased the venule diameter compared to saline. VEGFR2 antagonist on its own did not cause any alteration. Premedication with the antagonist or NO synthase blocker decreased the dilatory effect of VEGF significantly. However, in case of gingivitis significant venoconstriction occured for the VEGFR2 antagonist. Furthermore, VEGFR2 overexpressions were also detected both with immunohistochemical and western blot analysis. It is worth emphasizing that in gingivitis all components and neighboring cells of the vessel wall express conspicuously higher amount of VEGFR2. Conclusion: Our results demonstrate that functionally active VEGFR2s are located in the venules of rat healthy gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2 activation and consequent endothelium derived NO release pathway, shows venodilatory effects. Furthermore, both VEGF production and VEGFR2 expressions are increased in gingiva during gingivitis. We assume that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis and remodeling of the local microvascular network) of gingiva in inflammation. Inhibition of VEGFR2s may be a new therapeutic approach of periodontal disease.

UR - http://www.scopus.com/inward/record.url?scp=84892105494&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84892105494&partnerID=8YFLogxK

M3 - Chapter

SN - 9781626186552

SP - 153

EP - 167

BT - Vascular Endothelial Growth Factor (VEGF): Biology, Regulation and Clinical Significance

PB - Nova Science Publishers, Inc.

ER -