Transforming growth factor β1 down-regulates Runx-2 and alkaline phosphatase activity of human dental pulp cells via ALK5/Smad2/3 signaling

Po Shuen Lin, Mei Chi Chang, Chiu Po Chan, Sheng Yang Lee, Jang Jaer Lee, Yi Ling Tsai, Hui Chun Tseng, Tseng Fang Tai, Hsueh Jen Lin, Jiiang Huei Jeng

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Abstract

Objective Transforming growth factor β1 (TGF-β1) plays a role in repair and dentinogenesis in dental pulp. The purpose of this study was to study how TGF-β1 affects 2 differentiation markers, Runt-related transcription factor 2 (Runx-2) and ALP, in dental pulp cells. Study design Primary-cultured human dental pulp cells were treated with TGF-β1 with or without pretreatment and coincubation with 1,4-diamino-2,3-dicyano-1,4-bis(o- aminophenylmercapto)butadiene (U0126, a mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor), Noggin (a bone morphogenetic protein inhibitor), or 4-(5-benzol[1,3]dioxol-5-yl-4-pyrldin-2-yl- 1H-imidazol-2-yl)-benzamide hydrate (SB431542, an activin receptorlike kinase (ALK) 5/Smad2/3 inhibitor). The differentiation status of pulp cells was evaluated by ALP staining and quantitative ALP activity assay. Changes in ALP and Runx-2 mRNA expression were determined by reverse-transcription polymerase chain reaction. Results Cells under the treatment of TGF-β1 (5 and 10 ng/mL) showed a decrease in ALP activity and gene expression of ALP and Runx-2. Pretreatment by U0126 and Noggin was not effective to prevent the TGF-β1induced decline of ALP activity. Interestingly, SB431542 prevented the TGF-β1induced decline of ALP activity and ALP and Runx-2 gene expression. Conclusion TGF-β1 down-regulates Runx-2 and ALP in human dental pulp cells via ALK5/Smad2/3 signaling. These events may play important roles at specific stages of pulpal repair and dentinogenesis.

Original languageEnglish
Pages (from-to)394-400
Number of pages7
JournalOral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics
Volume111
Issue number3
DOIs
Publication statusPublished - Mar 2011

Fingerprint

Dental Pulp
Transforming Growth Factors
Human Activities
Alkaline Phosphatase
Down-Regulation
Dentinogenesis
Gene Expression
Bone Morphogenetic Proteins
Differentiation Antigens
Extracellular Signal-Regulated MAP Kinases
Benzene
Mitogens
Reverse Transcription
Transcription Factors
Phosphotransferases
Staining and Labeling
Polymerase Chain Reaction
Messenger RNA

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Surgery
  • Dentistry(all)
  • Oral Surgery

Cite this

Transforming growth factor β1 down-regulates Runx-2 and alkaline phosphatase activity of human dental pulp cells via ALK5/Smad2/3 signaling. / Lin, Po Shuen; Chang, Mei Chi; Chan, Chiu Po; Lee, Sheng Yang; Lee, Jang Jaer; Tsai, Yi Ling; Tseng, Hui Chun; Tai, Tseng Fang; Lin, Hsueh Jen; Jeng, Jiiang Huei.

In: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, Vol. 111, No. 3, 03.2011, p. 394-400.

Research output: Contribution to journalArticle

Lin, Po Shuen ; Chang, Mei Chi ; Chan, Chiu Po ; Lee, Sheng Yang ; Lee, Jang Jaer ; Tsai, Yi Ling ; Tseng, Hui Chun ; Tai, Tseng Fang ; Lin, Hsueh Jen ; Jeng, Jiiang Huei. / Transforming growth factor β1 down-regulates Runx-2 and alkaline phosphatase activity of human dental pulp cells via ALK5/Smad2/3 signaling. In: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2011 ; Vol. 111, No. 3. pp. 394-400.
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abstract = "Objective Transforming growth factor β1 (TGF-β1) plays a role in repair and dentinogenesis in dental pulp. The purpose of this study was to study how TGF-β1 affects 2 differentiation markers, Runt-related transcription factor 2 (Runx-2) and ALP, in dental pulp cells. Study design Primary-cultured human dental pulp cells were treated with TGF-β1 with or without pretreatment and coincubation with 1,4-diamino-2,3-dicyano-1,4-bis(o- aminophenylmercapto)butadiene (U0126, a mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor), Noggin (a bone morphogenetic protein inhibitor), or 4-(5-benzol[1,3]dioxol-5-yl-4-pyrldin-2-yl- 1H-imidazol-2-yl)-benzamide hydrate (SB431542, an activin receptorlike kinase (ALK) 5/Smad2/3 inhibitor). The differentiation status of pulp cells was evaluated by ALP staining and quantitative ALP activity assay. Changes in ALP and Runx-2 mRNA expression were determined by reverse-transcription polymerase chain reaction. Results Cells under the treatment of TGF-β1 (5 and 10 ng/mL) showed a decrease in ALP activity and gene expression of ALP and Runx-2. Pretreatment by U0126 and Noggin was not effective to prevent the TGF-β1induced decline of ALP activity. Interestingly, SB431542 prevented the TGF-β1induced decline of ALP activity and ALP and Runx-2 gene expression. Conclusion TGF-β1 down-regulates Runx-2 and ALP in human dental pulp cells via ALK5/Smad2/3 signaling. These events may play important roles at specific stages of pulpal repair and dentinogenesis.",
author = "Lin, {Po Shuen} and Chang, {Mei Chi} and Chan, {Chiu Po} and Lee, {Sheng Yang} and Lee, {Jang Jaer} and Tsai, {Yi Ling} and Tseng, {Hui Chun} and Tai, {Tseng Fang} and Lin, {Hsueh Jen} and Jeng, {Jiiang Huei}",
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T1 - Transforming growth factor β1 down-regulates Runx-2 and alkaline phosphatase activity of human dental pulp cells via ALK5/Smad2/3 signaling

AU - Lin, Po Shuen

AU - Chang, Mei Chi

AU - Chan, Chiu Po

AU - Lee, Sheng Yang

AU - Lee, Jang Jaer

AU - Tsai, Yi Ling

AU - Tseng, Hui Chun

AU - Tai, Tseng Fang

AU - Lin, Hsueh Jen

AU - Jeng, Jiiang Huei

PY - 2011/3

Y1 - 2011/3

N2 - Objective Transforming growth factor β1 (TGF-β1) plays a role in repair and dentinogenesis in dental pulp. The purpose of this study was to study how TGF-β1 affects 2 differentiation markers, Runt-related transcription factor 2 (Runx-2) and ALP, in dental pulp cells. Study design Primary-cultured human dental pulp cells were treated with TGF-β1 with or without pretreatment and coincubation with 1,4-diamino-2,3-dicyano-1,4-bis(o- aminophenylmercapto)butadiene (U0126, a mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor), Noggin (a bone morphogenetic protein inhibitor), or 4-(5-benzol[1,3]dioxol-5-yl-4-pyrldin-2-yl- 1H-imidazol-2-yl)-benzamide hydrate (SB431542, an activin receptorlike kinase (ALK) 5/Smad2/3 inhibitor). The differentiation status of pulp cells was evaluated by ALP staining and quantitative ALP activity assay. Changes in ALP and Runx-2 mRNA expression were determined by reverse-transcription polymerase chain reaction. Results Cells under the treatment of TGF-β1 (5 and 10 ng/mL) showed a decrease in ALP activity and gene expression of ALP and Runx-2. Pretreatment by U0126 and Noggin was not effective to prevent the TGF-β1induced decline of ALP activity. Interestingly, SB431542 prevented the TGF-β1induced decline of ALP activity and ALP and Runx-2 gene expression. Conclusion TGF-β1 down-regulates Runx-2 and ALP in human dental pulp cells via ALK5/Smad2/3 signaling. These events may play important roles at specific stages of pulpal repair and dentinogenesis.

AB - Objective Transforming growth factor β1 (TGF-β1) plays a role in repair and dentinogenesis in dental pulp. The purpose of this study was to study how TGF-β1 affects 2 differentiation markers, Runt-related transcription factor 2 (Runx-2) and ALP, in dental pulp cells. Study design Primary-cultured human dental pulp cells were treated with TGF-β1 with or without pretreatment and coincubation with 1,4-diamino-2,3-dicyano-1,4-bis(o- aminophenylmercapto)butadiene (U0126, a mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor), Noggin (a bone morphogenetic protein inhibitor), or 4-(5-benzol[1,3]dioxol-5-yl-4-pyrldin-2-yl- 1H-imidazol-2-yl)-benzamide hydrate (SB431542, an activin receptorlike kinase (ALK) 5/Smad2/3 inhibitor). The differentiation status of pulp cells was evaluated by ALP staining and quantitative ALP activity assay. Changes in ALP and Runx-2 mRNA expression were determined by reverse-transcription polymerase chain reaction. Results Cells under the treatment of TGF-β1 (5 and 10 ng/mL) showed a decrease in ALP activity and gene expression of ALP and Runx-2. Pretreatment by U0126 and Noggin was not effective to prevent the TGF-β1induced decline of ALP activity. Interestingly, SB431542 prevented the TGF-β1induced decline of ALP activity and ALP and Runx-2 gene expression. Conclusion TGF-β1 down-regulates Runx-2 and ALP in human dental pulp cells via ALK5/Smad2/3 signaling. These events may play important roles at specific stages of pulpal repair and dentinogenesis.

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