Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells

Shin Da Lee, Cheng Chung Wu, Yu Chao Chang, Sheng Huang Chang, Chieh Hsi Wu, Jia Ping Wu, Jin Ming Hwang, Wei Wen Kuo, Jer Yuh Liu, Chih Yang Huang

研究成果: 雜誌貢獻文章

13 引文 (Scopus)

摘要

Background: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. Methods: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. Results: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37%), U0126 (-35%), LY294002 (-49%), CsA (-49%), and SP600125 (-24%). Conclusions: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

原文英語
頁(從 - 到)684-691
頁數8
期刊Journal of Periodontology
77
發行號4
DOIs
出版狀態已發佈 - 四月 2006
對外發佈Yes

指紋

Porphyromonas gingivalis
Matrix Metalloproteinase 9
Hypertrophy
1-Phosphatidylinositol 4-Kinase
Phosphotransferases
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
Calcineurin
p38 Mitogen-Activated Protein Kinases
Cardiac Myocytes
Interleukin-10
Prevotella intermedia
Aggregatibacter actinomycetemcomitans
JNK Mitogen-Activated Protein Kinases
Periodontitis
Matrix Metalloproteinase 2
Mitogen-Activated Protein Kinase Kinases
Gelatin
Interleukin-1
Cyclosporine
Fluorescent Antibody Technique

ASJC Scopus subject areas

  • Dentistry(all)

引用此文

Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells. / Lee, Shin Da; Wu, Cheng Chung; Chang, Yu Chao; Chang, Sheng Huang; Wu, Chieh Hsi; Wu, Jia Ping; Hwang, Jin Ming; Kuo, Wei Wen; Liu, Jer Yuh; Huang, Chih Yang.

於: Journal of Periodontology, 卷 77, 編號 4, 04.2006, p. 684-691.

研究成果: 雜誌貢獻文章

Lee, Shin Da ; Wu, Cheng Chung ; Chang, Yu Chao ; Chang, Sheng Huang ; Wu, Chieh Hsi ; Wu, Jia Ping ; Hwang, Jin Ming ; Kuo, Wei Wen ; Liu, Jer Yuh ; Huang, Chih Yang. / Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells. 於: Journal of Periodontology. 2006 ; 卷 77, 編號 4. 頁 684-691.
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title = "Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells",
abstract = "Background: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. Methods: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. Results: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87{\%}) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37{\%}), U0126 (-35{\%}), LY294002 (-49{\%}), CsA (-49{\%}), and SP600125 (-24{\%}). Conclusions: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.",
keywords = "Cardiac cells, Hypertrophy, Matrix metalloproteinase, Periodontitis, Porphyromonas gingivalis, Signaling pathways",
author = "Lee, {Shin Da} and Wu, {Cheng Chung} and Chang, {Yu Chao} and Chang, {Sheng Huang} and Wu, {Chieh Hsi} and Wu, {Jia Ping} and Hwang, {Jin Ming} and Kuo, {Wei Wen} and Liu, {Jer Yuh} and Huang, {Chih Yang}",
year = "2006",
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pages = "684--691",
journal = "Journal of Periodontology",
issn = "0022-3492",
publisher = "American Academy of Periodontology",
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T1 - Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells

AU - Lee, Shin Da

AU - Wu, Cheng Chung

AU - Chang, Yu Chao

AU - Chang, Sheng Huang

AU - Wu, Chieh Hsi

AU - Wu, Jia Ping

AU - Hwang, Jin Ming

AU - Kuo, Wei Wen

AU - Liu, Jer Yuh

AU - Huang, Chih Yang

PY - 2006/4

Y1 - 2006/4

N2 - Background: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. Methods: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. Results: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37%), U0126 (-35%), LY294002 (-49%), CsA (-49%), and SP600125 (-24%). Conclusions: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

AB - Background: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. Methods: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. Results: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37%), U0126 (-35%), LY294002 (-49%), CsA (-49%), and SP600125 (-24%). Conclusions: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

KW - Cardiac cells

KW - Hypertrophy

KW - Matrix metalloproteinase

KW - Periodontitis

KW - Porphyromonas gingivalis

KW - Signaling pathways

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