Prostanoid- and interleukin-1-induced primary genes in cementoblastic cells

Jeanne Nervina, Paulo M. Camargo, Olga Bezouglaia, Sotirios Tetradis

Research output: Contribution to journalArticle

Abstract

Background: Cementum is a key component of a functional periodontal organ. However, regenerating lost cementum is difficult and often incomplete. Identifying molecular mediators of cementoblast differentiation and function should lead to better targeted treatment for periodontitis. Prostaglandins increase mineralization of murine cementoblastic OCCM cells and alveolar bone formation, whereas the cytokine interleukin-1 (IL-1) inhibits alveolar bone formation. We hypothesized that differentially induced primary genes in OCCM cells may mediate anabolic and catabolic responses. Our objective was to identify primary genes differentially induced by the synthetic prostanoid fluprostenol and IL-1 in cementoblastic cells. Methods: Confluent OCCM cells were pretreated with the protein synthesis inhibitor cycloheximide followed by fluprostenol or IL-1 for 1.5 hours. cDNA generated from each group was used for cDNA subtraction hybridization to identify differentially induced genes. Preferential gene induction was verified by Northern blot analysis. Results: Thirteen fluprostenol- and seven IL-1-regulated genes were identified. Among the fluprostenol-induced genes was mitogen-activated protein (MAP) kinase phosphatase 1 (MKP1), a negative regulator of MAP kinase signaling. To verify the cDNA subtraction hybridization results, OCCM cells were treated with fluprostenol or prostaglandin F (PGF), and MKP1 mRNA levels were determined. The 0.001 to 1 μM fluprostenol and 0.01 to 1 μM PGF significantly induced MKP1 mRNA levels, which peaked at 1 hour of treatment and returned to baseline at 2 hours. Conclusions: Fluprostenol enhanced, whereas IL-1 inhibited, OCCM mineralization. Using cDNA subtraction hybridization, we identified primary genes that correlate with the observed anabolic and catabolic responses. These findings further our understanding of cementoblast function and suggest that differentially induced genes may mediate cementum formation and resorption.

Original languageEnglish (US)
Pages (from-to)1362-1370
Number of pages9
JournalJournal of Periodontology
Volume77
Issue number8
DOIs
StatePublished - Aug 2006

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Interleukin-1
Prostaglandins
Dental Cementum
Dual Specificity Phosphatase 1
Genes
Complementary DNA
Dinoprost
Osteogenesis
Phosphotransferases
Mitogen-Activated Protein Kinase Phosphatases
Alveolar Epithelial Cells
Messenger RNA
Protein Synthesis Inhibitors
Periodontitis
Cycloheximide
fluprostenol
Mitogen-Activated Protein Kinases
Northern Blotting
Cytokines

Keywords

  • cDNA
  • Dental cementum
  • Fluprostenol
  • Genes
  • Hybridization
  • Interleukin-1

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Prostanoid- and interleukin-1-induced primary genes in cementoblastic cells. / Nervina, Jeanne; Camargo, Paulo M.; Bezouglaia, Olga; Tetradis, Sotirios.

In: Journal of Periodontology, Vol. 77, No. 8, 08.2006, p. 1362-1370.

Research output: Contribution to journalArticle

Nervina, J, Camargo, PM, Bezouglaia, O & Tetradis, S 2006, 'Prostanoid- and interleukin-1-induced primary genes in cementoblastic cells', Journal of Periodontology, vol. 77, no. 8, pp. 1362-1370. https://doi.org/10.1902/jop.2006.050354
Nervina, Jeanne ; Camargo, Paulo M. ; Bezouglaia, Olga ; Tetradis, Sotirios. / Prostanoid- and interleukin-1-induced primary genes in cementoblastic cells. In: Journal of Periodontology. 2006 ; Vol. 77, No. 8. pp. 1362-1370.
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AB - Background: Cementum is a key component of a functional periodontal organ. However, regenerating lost cementum is difficult and often incomplete. Identifying molecular mediators of cementoblast differentiation and function should lead to better targeted treatment for periodontitis. Prostaglandins increase mineralization of murine cementoblastic OCCM cells and alveolar bone formation, whereas the cytokine interleukin-1 (IL-1) inhibits alveolar bone formation. We hypothesized that differentially induced primary genes in OCCM cells may mediate anabolic and catabolic responses. Our objective was to identify primary genes differentially induced by the synthetic prostanoid fluprostenol and IL-1 in cementoblastic cells. Methods: Confluent OCCM cells were pretreated with the protein synthesis inhibitor cycloheximide followed by fluprostenol or IL-1 for 1.5 hours. cDNA generated from each group was used for cDNA subtraction hybridization to identify differentially induced genes. Preferential gene induction was verified by Northern blot analysis. Results: Thirteen fluprostenol- and seven IL-1-regulated genes were identified. Among the fluprostenol-induced genes was mitogen-activated protein (MAP) kinase phosphatase 1 (MKP1), a negative regulator of MAP kinase signaling. To verify the cDNA subtraction hybridization results, OCCM cells were treated with fluprostenol or prostaglandin F2α (PGF2α), and MKP1 mRNA levels were determined. The 0.001 to 1 μM fluprostenol and 0.01 to 1 μM PGF2α significantly induced MKP1 mRNA levels, which peaked at 1 hour of treatment and returned to baseline at 2 hours. Conclusions: Fluprostenol enhanced, whereas IL-1 inhibited, OCCM mineralization. Using cDNA subtraction hybridization, we identified primary genes that correlate with the observed anabolic and catabolic responses. These findings further our understanding of cementoblast function and suggest that differentially induced genes may mediate cementum formation and resorption.

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