Estrogen receptors and growth response in cultured human periodontal ligament cells

Lewko, Walter M.

doi:10.1016/0024-3205(86)90352-8

Cited by 21 publications

(12 citation statements)

References 19 publications

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“…1). [37][38][39]41,42 The possibility of additive effects from androgens plus P remains unresolved. They demonstrated that this effect was mediated by the androgen receptor, rather than the estrogen receptor which was also present in those cells.…”

Section: Discussionmentioning

confidence: 99%

Androgens Modulate Interleukin‐6 Production by Gingival Fibroblasts In Vitro

Gornstein

Lapp

Bustos‐Valdes

et al. 1999

Journal of Periodontology

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Section: Discussionmentioning

confidence: 99%

Androgens Modulate Interleukin‐6 Production by Gingival Fibroblasts In Vitro

Gornstein

Lapp

Bustos‐Valdes

et al. 1999

Journal of Periodontology

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“…In the periodontium, intracellular binding proteins have been partially characterized for estrogens (Vittek et al, 1982b;Musajo etal, 1984;Lewko and Anderson, 1986;Staffolani etal, 1989), androgens (Southern etal, 1978;Vittek etal, 1985), and progesterone (Vittek etal, 1982a). The human gingival cytosol receptor for estrogen is a highaffinity (Kd 340 jM), low-capacity (4.5 /mol/mg protein), heat-and proteolytic enzyme-sensitive protein that exhibits steroid specificity of binding to estradiol but not cortisol, progesterone, or testosterone (Vittek et al, 1982b).…”

Section: Sex Steroid Hormone Receptorsmentioning

confidence: 98%

Sex Steroid Hormones and Cell Dynamics in the Periodontium

Mariotti

1994

Critical Reviews in Oral Biology & Medicine

186

248

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The biological changes that occur in tissues of the periodontium during puberty, the menstrual cycle, pregnancy, menopause, and oral contraceptive use have heightened interest in the relationship between sex steroid hormones and periodontal health. These clinical observations coupled with tissue specificity of hormone localization, identification of hormone receptors, as well as the metabolism of hormones have strongly suggested that periodontal tissues are targets for androgens, estrogens, and progestins. The etiologies of periodontal endocrinopathies are diverse; nonetheless, periodontal pathologies may be a consequence of the actions and interactions of sex steroid hormones on specific cells found in the periodontium.

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“…Both ER subtypes are widely expressed in different cells and tissues and they show distinct and specific patterns of expression (1,2). Human periodontal ligament (PDL) cells have been shown to possess binding sites for radiolabelled 17β‐estradiol (E 2 ) and to express mRNA for ERs (3,4). We have shown that human PDL cells express preferentially ERβ immunoreactivity, while the signal for ERα is much lower, suggesting that PDL cells express predominantly ERβ protein (5,6).…”

mentioning

confidence: 99%

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

Nebel

Jönsson

Norderyd

et al. 2010

Journal of Periodontal Research

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Nebel D, Jönsson D, Norderyd O, Bratthall G, Nilsson B‐O. Differential regulation of chemokine expression by estrogen in human periodontal ligament cells. J Periodont Res 2010; 45: 796–802. © 2010 John Wiley & Sons A/S Background and Objective: Estrogen modulates inflammatory responses, but the mechanisms involved have not yet been identified. Periodontal ligament (PDL) cells produce chemokines (a group of chemoattractant molecules that recruit leukocytes) and it has been suggested that estrogen modulates periodontal inflammation by regulating the expression of chemokines by PDL cells. Therefore, the objectives of this study were to investigate the regulation of chemokine ligand 2 [CCL2/monocyte chemoattractant protein 1 (MCP‐1)], chemokine ligand 3 [CCL3/macrophage inflammatory protein‐1α (MIP‐1α)] and chemokine ligand 5 (CCL5/RANTES) by estrogen in human PDL cells. Material and Methods: PDL cells were obtained from the PDL of premolars, extracted for orthodontic reasons, from two boys and two girls (16 and 17 years of age). PDL cell CCL2, CCL3 and CCL5 mRNA transcripts were determined by quantitative real‐time PCR. The concentrations of CCL2, CCL3 and CCL5 proteins were determined by ELISAs. Results: Treatment with 0.5 μg/mL of lipopolysaccharide (LPS, from Escherichia coli) + 100 nm 17β‐estradiol (E2) for 24 h reduced the expression of CCL3 mRNA by about 40% compared to PDL cells treated with LPS alone. Attenuation of CCL3 mRNA was not associated with a decrease in CCL3 protein within 48 h, suggesting a slow turnover of the CCL3 protein. Interindividual differences in the effects of E2 on CCL5 mRNA expression were observed. E2 (100 nm) increased the expression of CCL5 by 40–60% in PDL cells derived from two subjects but reduced the expression of CCL5 by about 30% in cells from another subject. CCL2 mRNA and CCL2 protein were highly expressed, but not regulated by E2. Similar data were observed in cells obtained from both boys and girls. Conclusion: Regulation, by estrogen, of chemokine expression in PDL cells shows a complex pattern involving the down‐regulation as well as the up‐regulation of chemokines, suggesting that estrogen exerts both anti‐inflammatory and proinflammatory effects through these mechanisms.

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Estrogen receptors and growth response in cultured human periodontal ligament cells

Cited by 21 publications

References 19 publications

Androgens Modulate Interleukin‐6 Production by Gingival Fibroblasts In Vitro

Androgens Modulate Interleukin‐6 Production by Gingival Fibroblasts In Vitro

Sex Steroid Hormones and Cell Dynamics in the Periodontium

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

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