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Bradykinin inhibition of EGF- and PDGF-induced DNA synthesis in human fibroblasts

McAllister, B. S. ; Leeb-Lundberg, F. LU and Olson, M. S. (1993) In American Journal of Physiology: Cell Physiology 265(2 34-2). p.477-484
Abstract


Bradykinin exhibits proliferative influences in several types of cells; however, in the present study, bradykinin did not promote DNA synthesis but actually inhibited the DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) in human gingival fibroblasts (HGF). This dose-dependent inhibitory effect was a specific intracellular interaction in that increasing concentrations of EGF did not counteract the inhibitory actions of bradykinin when added at 100 nM. The phosphoinositide- calcium signaling cascade is a likely point of interaction for the inhibitory influences of bradykinin; however, no interactions between bradykinin and EGF were observed with the... (More)


Bradykinin exhibits proliferative influences in several types of cells; however, in the present study, bradykinin did not promote DNA synthesis but actually inhibited the DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) in human gingival fibroblasts (HGF). This dose-dependent inhibitory effect was a specific intracellular interaction in that increasing concentrations of EGF did not counteract the inhibitory actions of bradykinin when added at 100 nM. The phosphoinositide- calcium signaling cascade is a likely point of interaction for the inhibitory influences of bradykinin; however, no interactions between bradykinin and EGF were observed with the generation of inositol phosphates or intracellular calcium fluxes. The inhibitory influences of bradykinin do not appear to be the result of a transmodulation of the EGF receptor, since EGF-mediated autophosphorylation was not negatively affected by bradykinin. Bradykinin- stimulated prostaglandin E
2
(PGE
2
) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized. The results presented demonstrate that bradykinin can inhibit EGF- and PDGF-induced DNA synthesis and suggest that PGE
2
synthesis is responsible for the observed bradykinin inhibition of EGF- induced DNA synthesis.

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type
Contribution to journal
publication status
published
subject
keywords
epidermal growth factor, platelet-derived growth factor, prostaglandin E, signal transduction, thymidine incorporation
in
American Journal of Physiology: Cell Physiology
volume
265
issue
2 34-2
pages
477 - 484
publisher
American Physiological Society
external identifiers
  • scopus:0027240139
  • pmid:8396328
ISSN
1522-1563
language
English
LU publication?
no
id
b186c36a-9d60-44fa-a78a-7dda68b6c128
date added to LUP
2019-06-12 11:46:20
date last changed
2021-01-03 03:55:35
@article{b186c36a-9d60-44fa-a78a-7dda68b6c128,
  abstract     = {<p><br>
                            Bradykinin exhibits proliferative influences in several types of cells; however, in the present study, bradykinin did not promote DNA synthesis but actually inhibited the DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) in human gingival fibroblasts (HGF). This dose-dependent inhibitory effect was a specific intracellular interaction in that increasing concentrations of EGF did not counteract the inhibitory actions of bradykinin when added at 100 nM. The phosphoinositide- calcium signaling cascade is a likely point of interaction for the inhibitory influences of bradykinin; however, no interactions between bradykinin and EGF were observed with the generation of inositol phosphates or intracellular calcium fluxes. The inhibitory influences of bradykinin do not appear to be the result of a transmodulation of the EGF receptor, since EGF-mediated autophosphorylation was not negatively affected by bradykinin. Bradykinin- stimulated prostaglandin E<br>
                            <sub>2</sub><br>
                             (PGE<br>
                            <sub>2</sub><br>
                            ) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized. The results presented demonstrate that bradykinin can inhibit EGF- and PDGF-induced DNA synthesis and suggest that PGE<br>
                            <sub>2</sub><br>
                             synthesis is responsible for the observed bradykinin inhibition of EGF- induced DNA synthesis.<br>
                        </p>},
  author       = {McAllister, B. S. and Leeb-Lundberg, F. and Olson, M. S.},
  issn         = {1522-1563},
  language     = {eng},
  month        = {01},
  number       = {2 34-2},
  pages        = {477--484},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Cell Physiology},
  title        = {Bradykinin inhibition of EGF- and PDGF-induced DNA synthesis in human fibroblasts},
  volume       = {265},
  year         = {1993},
}