Cyclosporin A and hydroxycyclosporine (M-17) affect the secretory phenotype of human gingival fibroblasts.

doi:10.1111/J.1600-0714.1998.TB01953.X

Paper

Cyclosporin A and hydroxycyclosporine (M-17) affect the secretory phenotype of human gingival fibroblasts.

Published Feb 27, 2007 · A. Mariotti, T. Hassell, D. Jacobs

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology

Q1 SJR score

27

Citations

0

Influential Citations

Full textSemantic Scholar

Abstract

The responsiveness of human gingival fibroblast populations to cyclosporin A (CsA) and its principal metabolite, hydroxycyclosporine (M17), was evaluated in cell culture. Gingival fibroblasts exhibited a dose-dependent accumulation and bell-shaped distribution of dansylated CsA. A 100-fold excess of non-labeled CsA prevented the accumulation of the fluorescent probe in the fibroblasts. Both CsA (400 ng/ml) and M17 (100 ng/ml) stimulated mean gingival fibroblast cell number to 23.2% and 36.7% above controls, and reduced mean collagen production by 37.7% and 37.4% below controls, respectively; however, neither CsA nor M17 affected mean protein production in comparison to control cultures. Analyses of responses to CsA and M17 by ligand-accumulating and non-accumulating fibroblasts sorted out from the parent cultures did not provide consistent interstrain responses either by cells representing the upper quartile of fluorescence or cells representing the bottom quartiles of fluorescence. These data demonstrate that CsA is accumulated by gingival fibroblasts and that CsA and M17 are potent modulators of gingival fibroblast phenotype.

In Vitro Study

Study Snapshot

Cyclosporin A and its metabolite hydroxycyclosporine (M17) are potent modulators of gingival fibroblast phenotype, affecting cell number and collagen production without affecting protein production.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Sign up to use Study Snapshot

Consensus is limited without an account. Create an account or sign in to get more searches and use the Study Snapshot.

Create an account

Paper

Cyclosporin A and hydroxycyclosporine (M-17) affect the secretory phenotype of human gingival fibroblasts.

Sign up to use Study Snapshot

References

Oral lesions in organ transplant patients.

Organ transplant patients can experience oral problems such as hairy leukoplakia, increased infections, and lip cancer, highlighting the need for regular oral screening and team collaboration.

Cyclosporine A upregulates interleukin-6 gene expression in human gingiva: possible mechanism for gingival overgrowth.

Cyclosporine A therapy increases interleukin-6 protein and mRNA levels in overgrown human gingival tissues, potentially explaining the molecular mechanisms responsible for CsA-induced gingival overgrowth.

Comparative metabolism of 3H-glucosamine by fibroblast populations exposed to cyclosporine.

Cyclosporine and nifedipine therapy may cause gingival overgrowth by increasing fibroblast deposition of proteoglycans in the gingival extracellular matrix.

Cyclosporin A metabolism in human liver, kidney, and intestine slices. Comparison to rat and dog slices and human cell lines.

Cyclosporin A metabolism in human kidney and colonic mucosa contributes to the first-pass effect of the drug, with the liver being the major site of biotransformation and the human liver HepG2 cell line not suitable for this study.

Influence of cyclosporine a on growth and extracellular matrix synthesis of human fibroblasts

Cyclosporine A directly affects the proliferation of human gingival fibroblasts, potentially contributing to some of the observed hyperplasia in transplant recipients.

The effect of cyclosporin and lipopolysaccharide on fibroblasts: implications for cyclosporin-induced gingival overgrowth.

Cyclosporin-induced gingival overgrowth is influenced by bacterial lipopolysaccharide, which inhibits DNA synthesis and may contribute to the pathogenesis of this adverse side effect.

Cyclosporin-A increases type I procollagen production and mRNA level in human gingival fibroblasts in vitro.

Cyclosporine-A stimulates collagen synthesis in human gingival fibroblasts, but not DNA synthesis, suggesting a potential role in gingival overgrowth.

Identification of several cyclosporine binding proteins in lymphoid and non-lymphoid cells in vivo.

Cyclosporine A's intracellular targets and access to cyclophilin vary significantly in drug sensitive and resistant cell types, potentially explaining its lymphocyte selectivity.

Citations

Impact of Immunosuppressive Drugs on Fibroblasts: An In Vitro Study

Immunosuppressive drugs have distinct effects on fibroblast cell number, with their potential role in drug-induced gingival overgrowth being a multifactorial process.

Bibliometric analysis of research trends and characteristics of drug-induced gingival overgrowth

This bibliometric analysis reveals a growing interest in drug-induced gingival overgrowth (DIGO) research, with cyclosporine being the most commonly used drug and risk factors and pathogenesis being prominent topics.

Drug-Induced Gingival Overgrowth in an 8-Year-Old Girl: A Case Report

Drug-induced gingival overgrowth in a young girl with systemic lupus erythematosus can be caused by noninflammatory reactions to medications, chronic inflammation, or a combination of both factors.

Gingival overgrowth caused by Olmesartan Medoxomil: Observational study

Olmesartan Medoxomil, an antihypertensive agent, may cause mild gingival overgrowth in the upper and lower frontal dental elements, unrelated to other etiological factors.

Effects of cyclosporin, nifedipine and phenytoin on gingival myofibroblast transdifferentiation in monkeys

Cyclosporin, nifedipine, and phenytoin-induced gingival overgrowths in monkeys are not associated with myofibroblast transdifferentiation, proliferation, or apoptosis of gingival connective cells.