Inhibitory Effect of Panduratin A on c-Jun N-Terminal Kinase and Activator Protein-1 Signaling Involved in Porphyromonas gingivalis Supernatant-Stimulated Matrix Metalloproteinase-9 Expression in Human Oral Epidermoid Cells

Yanti, Yanti; Lee, Myoung-Su; Kim, Dae-Young; Hwang, Jae Kwan

doi:10.1248/bpb.32.1770

Cited by 17 publications

(10 citation statements)

References 31 publications

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“…Components of the Activator Protein (AP)-1 transcription factor complex jun B proto-oncogene (JUNB) and FBJ murine osteosarcoma viral oncogene homolog (c-Fos), were also increased at 6 h and 24 h. These findings are in agreement with earlier work demonstrating that P. gingivalis is able to activate the AP-1 transcription factor in osteoblasts, HUVEC’s and oral epidermoid cells [8], [110], [113].…”

Section: Resultssupporting

confidence: 91%

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Reddi

Belibasakis

2012

PLoS ONE

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Periodontitis is an infectious inflammatory disease that destroys the tooth-supporting (periodontal) tissues. Porphyromonas gingivalis is an oral pathogen highly implicated in the pathogenesis of this disease. It can exert its effects to a number of cells, including osteogenic bone marrow stromal cells which are important for homeostastic capacity of the tissues. By employing gene microarray technology, this study aimed to describe the overall transcriptional events (>2-fold regulation) elicited by P. gingivalis secreted products in bone marrow stromal cells, and to dissect further the categories of genes involved in bone metabolism, inflammatory and immune responses. After 6 h of challenge with P. gingivalis, 271 genes were up-regulated whereas 209 genes were down-regulated, whereas after 24 h, these numbers were 259 and 109, respectively. The early (6 h) response was characterised by regulation of genes associated with inhibition of cell cycle, induction of apoptosis and loss of structural integrity, whereas the late (24 h) response was characterised by induction of chemokines, cytokines and their associated intracellular pathways (such as NF-κB), mediators of connective tissue and bone destruction, and suppression of regulators of osteogenic differentiation. The most strongly up-regulated genes were lipocalin 2 (LCN2) and serum amyloid A3 (SAA3), both encoding for proteins of the acute phase inflammatory response. Collectively, these transcriptional changes elicited by P. gingivalis denote that the fundamental cellular functions are hindered, and that the cells acquire a phenotype commensurate with propagated innate immune response and inflammatory-mediated tissue destruction. In conclusion, the global transcriptional profile of bone marrow stromal cells in response to P. gingivalis is marked by deregulated homeostatic functions, with implications in the pathogenesis of periodontitis.

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Section: Resultssupporting

confidence: 91%

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Reddi

Belibasakis

2012

PLoS ONE

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“…However, as stimulation of epithelial cells with heat-killed P. gingivalis does not regulate miR-203 (7), it would appear that viable bacteria are required and that induction may be related to an aspect of the process of internalization or intracellular adaptation. Transcription factors AP-1, SP1, and NF-B can control expression of miR-203 (39,50), and although viable P. gingivalis cells do not activate NF-B in GECs (57), the organism can activate AP-1 in HeLa cells (59) and SP1 in monocytes (15). Activation of AP-1 can occur through the protein kinase C (PKC) pathway, and inhibitors of PKC abrogate expression of miR-203 (50).…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Induction of MicroRNA-203 Expression Controls Suppressor of Cytokine Signaling 3 in Gingival Epithelial Cells

2011

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Porphyromonas gingivalis is a pathogen in severe periodontal disease. Able to exploit an intracellular lifestyle within primary gingival epithelial cells (GECs), a reservoir of P. gingivalis can persist within the gingival epithelia. This process is facilitated by manipulation of the host cell signal transduction cascades which can impact cell cycle, cell death, and cytokine responses. Using microarrays, we investigated the ability of P. gingivalis 33277 to regulate microRNA (

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“…Yanti et al [8] demonstrated that panduratin A showed a dose-dependent effect in preventing and reducing the biofilm. The result suggests that panduratin A is applicable as a natural anti-biofilm.…”

Section: Introductionmentioning

confidence: 99%

Identification and antioxidant activity test of bioactive compound produced from ethanol extract of temukunci (Boesenbergia rotunda)

Atun¹,

Handayani²,

Frindryani³

2017

AIP Conference Proceedings

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Inhibitory Effect of Panduratin A on c-Jun N-Terminal Kinase and Activator Protein-1 Signaling Involved in Porphyromonas gingivalis Supernatant-Stimulated Matrix Metalloproteinase-9 Expression in Human Oral Epidermoid Cells

Cited by 17 publications

References 31 publications

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Porphyromonas gingivalis Induction of MicroRNA-203 Expression Controls Suppressor of Cytokine Signaling 3 in Gingival Epithelial Cells

Identification and antioxidant activity test of bioactive compound produced from ethanol extract of temukunci (Boesenbergia rotunda)

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