Expression of endothelin‐1 in gingival epithelial cells

Yamamoto, Eri; Awano, Shuji; Koseki, Takeyoshi; Ansai, Toshihiro; Takehara, Tadamichi

doi:10.1034/j.1600-0765.2003.00668.x

Cited by 30 publications

(31 citation statements)

References 29 publications

(33 reference statements)

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“…ET-1 has been found to be expressed in normal striated duct cells (but not in the acinar cells or intercalated cells) 19 and in normal gingival epithelial cells. 20 An Increased ET-1 level was reported in the cell culture system when gingival epithelial cells were infected by periodontopathic bacteria. 21 Therefore, any factor that can affect secretion of ET-1 from the striated duct cells or the gingival epithelial cells can also potentially affect the salivary ET-1 level.…”

Section: Discussionmentioning

confidence: 99%

Salivary endothelin-1 potential for detecting oral cancer in patients with oral lichen planus or oral cancer in remission

et al. 2011

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Objectives Endothelin-1 (ET-1) is a potent vasoconstrictor involved not only in vascular biology but also in carcinogenesis. Results of a study in 2007 suggested salivary ET-1 as a potential biomarker for oral squamous cell carcinoma (OSCC), but a later study showed conflicting results. The purpose of our pilot study was to investigate feasibility of using salivary ET-1 as a biomarker for OSCC in two groups: oral lichen planus (OLP) patients and patients with OSCC in remission. Materials and Methods Saliva samples were collected from five groups of subjects: patients with newly diagnosed, active OSCC (Group A); patients with OSCC in remission (Group B); patients with active OLP lesions (Group C); patients with OLP in remission (Group D); and normal controls (Group E). Salivary ET-1 levels were determined by enzyme-linked immunosorbent assay, and the results were analyzed by the Mann Whitney U test. Results The mean salivary ET-1 level in Group A was significantly higher than that found in Group C (p=0.001), Group D (p=0.015) or Group E (p=0.004). There were no significant differences (p>0.05) in the mean salivary ET-1 levels between Groups A and B; Groups B and C; Groups B and D; Groups B and E; Groups C and D; Groups C and E; or Groups D and E. Conclusion Salivary ET-1 could be a good biomarker for OSCC development in OLP patients regardless of the degree of OLP disease activity. However, it appeared not to be a good biomarker for detecting recurrence of OSCC in patients in remission.

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Section: Discussionmentioning

confidence: 99%

Salivary endothelin-1 potential for detecting oral cancer in patients with oral lichen planus or oral cancer in remission

et al. 2011

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“…ET-1 is a powerful vasoconstrictor with mitogenic activity on vascular smooth muscle and fibroblasts. There are currently two distinct human endothelin receptors known, ETA and ETB, which are members of the seven transmembrane G protein-coupled rhodopsin superfamily [62, 63]. Activation of both ETA and ETB on smooth muscle cells leads to vasoconstriction, whereas activation of ETB located on endothelial cells leads to vasodilation by increasing NO production [64].…”

Section: Endothelin and Mast Cellmentioning

confidence: 99%

Influence of Mast Cells in Drug-Induced Gingival Overgrowth

Subramani

Rathnavelu

Yeap

et al. 2013

Mediators of Inflammation

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Mast cells (MCs) are multifunctional effector cells that were originally thought to be involved in allergic disorders. Now it is known that they contain an array of mediators with a multitude of effects on many other cells. MCs have become a recent concern in drug-induced gingival overgrowth (DIGO), an unwanted outcome of systemic medication. Most of the studies have confirmed the significant presence of inflammation as a prerequisite for the overgrowth to occur. The inflammatory changes within the gingival tissue appear to influence the interaction between the inducing drug and the fibroblast activity. The development of antibodies to MC-specific enzymes, tryptase and chymase, has facilitated the study of mast cells in DIGO. Many immunohistochemical studies involving MCs have been conducted; as a result, DIGO tissues are found to have increased the number of MCs in the gingiva, especially in the area of fibrosis. At the cellular level, gingival fibrogenesis is initiated by several mediators which induce the recruitment of a large number of inflammatory cells, including MCs. The purpose of this paper is to access the roles played by MCs in gingival overgrowth to hypothesize a relationship between these highly specialized cells in the pathogenesis of DIGO.

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“…In addition, ET-1 expression is strongly induced by P . gingivalis in KB cells and HEp-2 cells [6, 10]. …”

Section: Introductionmentioning

confidence: 99%

“…gingivalis infection and in subsequent inflammatory responses that lead to periodontitis. However, most of the studies discussed have been conducted with the epidermoid carcinoma cell line, KB, and the larynx carcinoma cell line, HEp-2 [6, 8, 10]. Unfortunately, these cell lines are contaminated with the cervical adenocarcinoma cell line, HeLa [11, 12].…”

Section: Introductionmentioning

confidence: 99%

Endothelin Regulates Porphyromonas gingivalis-Induced Production of Inflammatory Cytokines

Son

Bak

Kim³

et al. 2016

PLoS ONE

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Periodontitis is a very common oral inflammatory disease that results in the destruction of supporting connective and osseous tissues of the teeth. Although the exact etiology is still unclear, Gram-negative bacteria, especially Porphyromonas gingivalis in subgingival pockets are thought to be one of the major etiologic agents of periodontitis. Endothelin (ET) is a family of three 21-amino acid peptides, ET-1, -2, and -3, that activate G protein-coupled receptors, ETA and ETB. Endothelin is involved in the occurrence and progression of various inflammatory diseases. Previous reports have shown that ET-1 and its receptors, ETA and ETB are expressed in the periodontal tissues and, that ET-1 levels in gingival crevicular fluid are increased in periodontitis patients. Moreover, P. gingivalis infection has been shown to induce the production of ET-1 along with other inflammatory cytokines. Despite these studies, however, the functional significance of endothelin in periodontitis is still largely unknown. In this study, we explored the cellular and molecular mechanisms of ET-1 action in periodontitis using human gingival epithelial cells (HGECs). ET-1 and ETA, but not ETB, were abundantly expressed in HGECs. Stimulation of HGECs with P. gingivalis or P. gingivalis lipopolysaccharide increased the expression of ET-1 and ETA suggesting the activation of the endothelin signaling pathway. Production of inflammatory cytokines, IL-1β, TNFα, and IL-6, was significantly enhanced by exogenous ET-1 treatment, and this effect depended on the mitogen-activated protein kinases via intracellular Ca2+ increase, which resulted from the activation of the phospholipase C/inositol 1,4,5-trisphosphate pathway. The inhibition of the endothelin receptor-mediated signaling pathway with the dual receptor inhibitor, bosentan, partially ameliorated alveolar bone loss and immune cell infiltration. These results suggest that endothelin plays an important role in P. gingivalis-mediated periodontitis. Thus, endothelin antagonism may be a potential therapeutic approach for periodontitis treatment.

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Expression of endothelin‐1 in gingival epithelial cells

Abstract: These results suggested that the expression level of ET-1 in gingival epithelial cells might be enhanced during the periodontal inflammation.

Cited by 30 publications

References 29 publications

Salivary endothelin-1 potential for detecting oral cancer in patients with oral lichen planus or oral cancer in remission

Salivary endothelin-1 potential for detecting oral cancer in patients with oral lichen planus or oral cancer in remission

Influence of Mast Cells in Drug-Induced Gingival Overgrowth

Endothelin Regulates Porphyromonas gingivalis-Induced Production of Inflammatory Cytokines

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