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The functional interaction of EGF and PDGF with bradykinin in the proliferation of human gingival fibroblasts.

McAllister, B. S. ; Leeb-Lundberg, F. LU ; Mellonig, J. T. and Olson, M. S. (1995) In Journal of Periodontology 66(6). p.429-437
Abstract

Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-BB are both involved in periodontal wound healing. Each of these growth factors exerts a positive proliferative effect on cells of the periodontium in vitro. However, in vivo the peptide bradykinin is one of a complex array of mediators present in addition to these growth factors. The purposes of this investigation were to: 1) evaluate bradykinin interactions with EGF and PDGF-BB altering cell proliferation in cultured human gingival fibroblasts (HGF), periodontal ligament cells (HPDL), and cells derived from alveolar bone (HOB); and 2) determine at the signal transduction level the mechanism of interaction between EGF and bradykinin in HGF. EGF and PDGF-BB... (More)

Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-BB are both involved in periodontal wound healing. Each of these growth factors exerts a positive proliferative effect on cells of the periodontium in vitro. However, in vivo the peptide bradykinin is one of a complex array of mediators present in addition to these growth factors. The purposes of this investigation were to: 1) evaluate bradykinin interactions with EGF and PDGF-BB altering cell proliferation in cultured human gingival fibroblasts (HGF), periodontal ligament cells (HPDL), and cells derived from alveolar bone (HOB); and 2) determine at the signal transduction level the mechanism of interaction between EGF and bradykinin in HGF. EGF and PDGF-BB stimulated DNA synthesis in a concentration-dependent manner, as measured by [3H] thymidine incorporation. Bradykinin alone did not alter significantly based DNA synthesis values; however, bradykinin in combination with EGF reduced DNA synthesis to nearly basal levels and bradykinin in combination with PDGF reduced the DNA synthesis over 50%. Examination of the interactions between bradykinin and EGF signal transduction pathways revealed that PGE2 release was increased in the presence of bradykinin and EGF (167 +/- 33% to 317 +/- 29%). The bradykinin-stimulated PGE2 release was completely abolished by indomethacin. Indomethacin also was found to block the bradykinin inhibition of EGF-induced DNA synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

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author
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publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Periodontology
volume
66
issue
6
pages
429 - 437
publisher
American Academy of Periodontology
external identifiers
  • scopus:0029320264
  • pmid:7562331
ISSN
0022-3492
DOI
10.1902/jop.1995.66.6.429
language
English
LU publication?
no
id
6e0bc670-73e5-433d-9da2-a1412a786f15
date added to LUP
2019-06-12 11:38:44
date last changed
2021-01-03 08:48:38
@article{6e0bc670-73e5-433d-9da2-a1412a786f15,
  abstract     = {<p>Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-BB are both involved in periodontal wound healing. Each of these growth factors exerts a positive proliferative effect on cells of the periodontium in vitro. However, in vivo the peptide bradykinin is one of a complex array of mediators present in addition to these growth factors. The purposes of this investigation were to: 1) evaluate bradykinin interactions with EGF and PDGF-BB altering cell proliferation in cultured human gingival fibroblasts (HGF), periodontal ligament cells (HPDL), and cells derived from alveolar bone (HOB); and 2) determine at the signal transduction level the mechanism of interaction between EGF and bradykinin in HGF. EGF and PDGF-BB stimulated DNA synthesis in a concentration-dependent manner, as measured by [3H] thymidine incorporation. Bradykinin alone did not alter significantly based DNA synthesis values; however, bradykinin in combination with EGF reduced DNA synthesis to nearly basal levels and bradykinin in combination with PDGF reduced the DNA synthesis over 50%. Examination of the interactions between bradykinin and EGF signal transduction pathways revealed that PGE2 release was increased in the presence of bradykinin and EGF (167 +/- 33% to 317 +/- 29%). The bradykinin-stimulated PGE2 release was completely abolished by indomethacin. Indomethacin also was found to block the bradykinin inhibition of EGF-induced DNA synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)</p>},
  author       = {McAllister, B. S. and Leeb-Lundberg, F. and Mellonig, J. T. and Olson, M. S.},
  issn         = {0022-3492},
  language     = {eng},
  month        = {01},
  number       = {6},
  pages        = {429--437},
  publisher    = {American Academy of Periodontology},
  series       = {Journal of Periodontology},
  title        = {The functional interaction of EGF and PDGF with bradykinin in the proliferation of human gingival fibroblasts.},
  url          = {http://dx.doi.org/10.1902/jop.1995.66.6.429},
  doi          = {10.1902/jop.1995.66.6.429},
  volume       = {66},
  year         = {1995},
}