The up‐regulation of heme oxygenase‐1 expression in human gingival fibroblasts stimulated with nicotine

Chang, Yu‐Chao; Lai, Chih Cheng; Lin, Li-Fen; Ni, Wei-Fen; Tsai, Cheng-Han

doi:10.1111/j.1600-0765.2005.00804.x

Cited by 43 publications

(44 citation statements)

References 35 publications

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“…As shown in Fig. 1, HO-1 expression is generally low in normal oral mucosa and is exclusively limited to actively differentiating basal cells, which is similar to the results reported by CHANG et al 2 . In the present study, HO-1 positive cells were mainly found in basal and parabasal cells of the dysplastic epithelium and in cancerous cells.…”

Section: Discussionsupporting

confidence: 88%

Upregulation of heme oxygenase-1 in oral epithelial dysplasias

Lee

et al. 2008

International Journal of Oral and Maxillofacial Surgery

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Section: Discussionsupporting

confidence: 88%

Upregulation of heme oxygenase-1 in oral epithelial dysplasias

Lee

et al. 2008

International Journal of Oral and Maxillofacial Surgery

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“…Although previous studies reported that nicotine causes injury to periodontal ligament cells via multiple mechanisms, including c-Fos, COX-2, heme oxygenase-1 and oxidative stress [22][23][24] , the molecular mechanisms of these effects have not been fully elucidated. Elevated P.…”

Section: Discussionmentioning

confidence: 99%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and PGE2 and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and PGE2 release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

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“…The mechanism of activation in this case is proposed to be through reduced hepatocyte production of reactive oxygen species and subsequent reduction in cellular oxidative stress (48), mechanisms of cell damage that may be activated by ricin. Nicotine's effect on antioxidant systems is complex, with reports of decreased activities of antioxidant enzymes such as glutathione peroxidase and catalase, but nicotine has also been shown to upregulate expression of heme oxygenase-1, a stress-inducible protein that functions as an antioxidant enzyme (49), as well as superoxide dismutase levels in the kidney (50). With ricin having significant prooxidant effects (26,30,51), any protective antioxidant enzymes that may be induced by nicotine may prove effective in maintaining organ function following ricin exposure.…”

Section: Discussionmentioning

confidence: 99%

Activation of the Cholinergic Antiinflammatory Pathway Reduces Ricin-Induced Mortality and Organ Failure in Mice

Mabley

Pacher

Szabó

2009

Mol Med

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Exposure to ricin, either by accident through ingestion of castor oil plant seeds or intentionally through its use as a bioweapon, invariably leads to multiple organ damage and death. Currently there is only a vaccine in advanced development to ricin, but no other antidote. Ricin causes systemic inflammation with increased proinflammatory cytokine release and subsequent multiple organ failure, particularly kidney and liver dysfunction. Activation of the cholinergic antiinflammatory pathway, specifically through the alpha7 nicotinic acetylcholine receptor (either indirectly through vagus nerve stimulation or directly through nicotine treatment) reduces proinflammatory gene expression. This activation also increases release of proinflammatory chemokines and cytokines, and has proven effective in a variety of inflammatory diseases. The aim of this study was to investigate whether nicotine treatment protected against ricin toxicity in mice. Male Balb/c mice exposed to ricin had increased serum levels of the inflammatory cytokine tumor necrosis factor-α and markers of both kidney (blood urea nitrogen, creatine) and liver (alanine tranaminase) dysfunction, with a subsequent increase in mortality. Nicotine administration 2 h after ricin injection significantly delayed and reduced ricin-induced mortality, an effect coupled with reduced serum levels of tumor necrosis factor-α and markers of kidney and liver dysfunction. Both the kidney and liver had markedly increased cellular oxidative stress following ricin exposure, an effect attenuated by nicotine administration. In conclusion, these data demonstrate that in cases of ricin poisoning, activation of the cholinergic antiinflammatory pathway may prove beneficial by reducing organ damage, delaying mortality, and allowing for a greater chance of survival.

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The up‐regulation of heme oxygenase‐1 expression in human gingival fibroblasts stimulated with nicotine

Cited by 43 publications

References 35 publications

Upregulation of heme oxygenase-1 in oral epithelial dysplasias

Upregulation of heme oxygenase-1 in oral epithelial dysplasias

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Activation of the Cholinergic Antiinflammatory Pathway Reduces Ricin-Induced Mortality and Organ Failure in Mice

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