Platelet-derived growth factor-BB stimulated cell migration mediated through p38 signal transduction pathway in periodontal cells

Angel K. Ray, Anne C Jones, David L. Carnes, David L Cochran, James T. Mellonig, Thomas W. Oates

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Background: Intracellular signaling pathways mediate specific responses to growth factors. The manipulation of these pathways ultimately may be used to control the clinical outcomes of periodontal regenerative therapy. The purpose of this study was to examine the role of the p38 signal transduction pathway in the responses of periodontal cells to platelet-derived growth factor-BB (PDGF). Methods: Primary cultures of human periodontal ligament cells (PDLs) and gingival fibroblasts (GFs) were used for all experiments. Cell numbers, 3H-thymidine incorporation, and Boyden chamber assays were used to characterize the effects of SB 203580 (SB), a specific inhibitor of the p38 signaling pathway, on cell proliferation and migration. An in vitro wound model also was used to assess the effects of SB. For the in vitro wound assay, triplicate wells were incubated for 1, 3, 5, and 7 days using 0.1% fetal bovine serum (FBS), 10% FBS ± 10 μM SB, or 20 ng/ml PDGF ± 10 μM SB. Digital histomorphometric analysis assessed cellular fill within the wound area. Results: SB specifically inhibited PDGF-induced migration in the Boyden chamber assays without affecting cell proliferation. The wound model data showed similar levels of wound fill for PDLs and GFs in 10% FBS. Relative to 10% FBS, PDLs stimulated with PDGF showed significantly (P<0.01, analysis of variance) greater wound fill (74%) than GFs (12%). SB inhibited the PDGF-induced wound fill of PDLs and GFs by 64% and 57%, respectively. This inhibition was significant (P<0.01, ANOVA) only for PDLs. The addition of SB to 10% FBS did not significantly affect the wound fill response of either cell type compared to 10% FBS alone. Conclusions: These results demonstrate that periodontal cells possess distinct responses to PDGF that may be altered at the signal transduction level. The manipulation of these responses through the use of inhibitors to specific signaling pathways may enhance our control of periodontal regeneration in the future.

Original languageEnglish (US)
Pages (from-to)1320-1328
Number of pages9
JournalJournal of Periodontology
Volume74
Issue number9
DOIs
StatePublished - Sep 2003

Fingerprint

Cell Movement
Signal Transduction
Periodontal Ligament
Wounds and Injuries
Fibroblasts
Serum
Analysis of Variance
Cell Proliferation
platelet-derived growth factor BB
Thymidine
Regeneration
Intercellular Signaling Peptides and Proteins
Cell Count

Keywords

  • Cells, periodontal
  • Fibroblasts, gingival
  • Growth factor, platelet-derived
  • Periodontal regeneration
  • Signal transduction

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Platelet-derived growth factor-BB stimulated cell migration mediated through p38 signal transduction pathway in periodontal cells. / Ray, Angel K.; Jones, Anne C; Carnes, David L.; Cochran, David L; Mellonig, James T.; Oates, Thomas W.

In: Journal of Periodontology, Vol. 74, No. 9, 09.2003, p. 1320-1328.

Research output: Contribution to journalArticle

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title = "Platelet-derived growth factor-BB stimulated cell migration mediated through p38 signal transduction pathway in periodontal cells",
abstract = "Background: Intracellular signaling pathways mediate specific responses to growth factors. The manipulation of these pathways ultimately may be used to control the clinical outcomes of periodontal regenerative therapy. The purpose of this study was to examine the role of the p38 signal transduction pathway in the responses of periodontal cells to platelet-derived growth factor-BB (PDGF). Methods: Primary cultures of human periodontal ligament cells (PDLs) and gingival fibroblasts (GFs) were used for all experiments. Cell numbers, 3H-thymidine incorporation, and Boyden chamber assays were used to characterize the effects of SB 203580 (SB), a specific inhibitor of the p38 signaling pathway, on cell proliferation and migration. An in vitro wound model also was used to assess the effects of SB. For the in vitro wound assay, triplicate wells were incubated for 1, 3, 5, and 7 days using 0.1{\%} fetal bovine serum (FBS), 10{\%} FBS ± 10 μM SB, or 20 ng/ml PDGF ± 10 μM SB. Digital histomorphometric analysis assessed cellular fill within the wound area. Results: SB specifically inhibited PDGF-induced migration in the Boyden chamber assays without affecting cell proliferation. The wound model data showed similar levels of wound fill for PDLs and GFs in 10{\%} FBS. Relative to 10{\%} FBS, PDLs stimulated with PDGF showed significantly (P<0.01, analysis of variance) greater wound fill (74{\%}) than GFs (12{\%}). SB inhibited the PDGF-induced wound fill of PDLs and GFs by 64{\%} and 57{\%}, respectively. This inhibition was significant (P<0.01, ANOVA) only for PDLs. The addition of SB to 10{\%} FBS did not significantly affect the wound fill response of either cell type compared to 10{\%} FBS alone. Conclusions: These results demonstrate that periodontal cells possess distinct responses to PDGF that may be altered at the signal transduction level. The manipulation of these responses through the use of inhibitors to specific signaling pathways may enhance our control of periodontal regeneration in the future.",
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AU - Ray, Angel K.

AU - Jones, Anne C

AU - Carnes, David L.

AU - Cochran, David L

AU - Mellonig, James T.

AU - Oates, Thomas W.

PY - 2003/9

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N2 - Background: Intracellular signaling pathways mediate specific responses to growth factors. The manipulation of these pathways ultimately may be used to control the clinical outcomes of periodontal regenerative therapy. The purpose of this study was to examine the role of the p38 signal transduction pathway in the responses of periodontal cells to platelet-derived growth factor-BB (PDGF). Methods: Primary cultures of human periodontal ligament cells (PDLs) and gingival fibroblasts (GFs) were used for all experiments. Cell numbers, 3H-thymidine incorporation, and Boyden chamber assays were used to characterize the effects of SB 203580 (SB), a specific inhibitor of the p38 signaling pathway, on cell proliferation and migration. An in vitro wound model also was used to assess the effects of SB. For the in vitro wound assay, triplicate wells were incubated for 1, 3, 5, and 7 days using 0.1% fetal bovine serum (FBS), 10% FBS ± 10 μM SB, or 20 ng/ml PDGF ± 10 μM SB. Digital histomorphometric analysis assessed cellular fill within the wound area. Results: SB specifically inhibited PDGF-induced migration in the Boyden chamber assays without affecting cell proliferation. The wound model data showed similar levels of wound fill for PDLs and GFs in 10% FBS. Relative to 10% FBS, PDLs stimulated with PDGF showed significantly (P<0.01, analysis of variance) greater wound fill (74%) than GFs (12%). SB inhibited the PDGF-induced wound fill of PDLs and GFs by 64% and 57%, respectively. This inhibition was significant (P<0.01, ANOVA) only for PDLs. The addition of SB to 10% FBS did not significantly affect the wound fill response of either cell type compared to 10% FBS alone. Conclusions: These results demonstrate that periodontal cells possess distinct responses to PDGF that may be altered at the signal transduction level. The manipulation of these responses through the use of inhibitors to specific signaling pathways may enhance our control of periodontal regeneration in the future.

AB - Background: Intracellular signaling pathways mediate specific responses to growth factors. The manipulation of these pathways ultimately may be used to control the clinical outcomes of periodontal regenerative therapy. The purpose of this study was to examine the role of the p38 signal transduction pathway in the responses of periodontal cells to platelet-derived growth factor-BB (PDGF). Methods: Primary cultures of human periodontal ligament cells (PDLs) and gingival fibroblasts (GFs) were used for all experiments. Cell numbers, 3H-thymidine incorporation, and Boyden chamber assays were used to characterize the effects of SB 203580 (SB), a specific inhibitor of the p38 signaling pathway, on cell proliferation and migration. An in vitro wound model also was used to assess the effects of SB. For the in vitro wound assay, triplicate wells were incubated for 1, 3, 5, and 7 days using 0.1% fetal bovine serum (FBS), 10% FBS ± 10 μM SB, or 20 ng/ml PDGF ± 10 μM SB. Digital histomorphometric analysis assessed cellular fill within the wound area. Results: SB specifically inhibited PDGF-induced migration in the Boyden chamber assays without affecting cell proliferation. The wound model data showed similar levels of wound fill for PDLs and GFs in 10% FBS. Relative to 10% FBS, PDLs stimulated with PDGF showed significantly (P<0.01, analysis of variance) greater wound fill (74%) than GFs (12%). SB inhibited the PDGF-induced wound fill of PDLs and GFs by 64% and 57%, respectively. This inhibition was significant (P<0.01, ANOVA) only for PDLs. The addition of SB to 10% FBS did not significantly affect the wound fill response of either cell type compared to 10% FBS alone. Conclusions: These results demonstrate that periodontal cells possess distinct responses to PDGF that may be altered at the signal transduction level. The manipulation of these responses through the use of inhibitors to specific signaling pathways may enhance our control of periodontal regeneration in the future.

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KW - Fibroblasts, gingival

KW - Growth factor, platelet-derived

KW - Periodontal regeneration

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