Inhibition by nifedipine of adherence- and activated macrophage-induced death of human gingival fibroblasts

Fujimori, Yasushi; Maeda, Shin; Saeki, Makio; Morisaki, Ichijiro; Kamisaki, Yoshínori

doi:10.1016/s0014-2999(01)00810-x

Cited by 27 publications

(27 citation statements)

References 26 publications

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“…Murine macrophage-like RAW264.7 cells were cultured as described previously (Fujimori, et al, 2001). Briefly, the cells were grown in Dulbecco's modified Eagle's medium supplemented with 10% FCS, 4 mM L-glutamine, 100 units/mL penicillin, 0.1 mg/mL streptomycin, and 12.5 units/mL nystatin.…”

Section: Methodsmentioning

confidence: 99%

Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model

Lifshitz

Weiss

Benromano

et al. 2012

Neurobiology of Aging

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Cerebrovascular amyloidosis is caused by amyloid accumulation in walls of blood vessel walls leading to hemorrhagic stroke and cognitive impairment. Transforming growth factor-β1 (TGF-β1) expression levels correlate with the degree of cerebrovascular amyloid deposition in Alzheimer s disease (AD) and TGF-β1 immunoreactivity in such cases is increased along the cerebral blood vessels. Here we show that a nasally administered proteosome-based adjuvant activates macrophages and decreases vascular amyloid in TGF-β1 mice. Animals were nasally treated with a proteosome-based adjuvant on a weekly basis for three months beginning at age 13 months. Using MRI we found that while control animals showed a significant cerebrovascular pathology, proteosome-based adjuvant prevents further brain damage and prevents pathological changes in the blood-brain barrier. Using an object recognition test and Y-maze, we found significant improvement in cognition in the treated group. Our findings support the potential use of a macrophage immuno-modulator as a novel approach to reduce cerebrovascular amyloid, prevent microhemorrhage and improve cognition.

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Section: Methodsmentioning

confidence: 99%

Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model

Lifshitz

Weiss

Benromano

et al. 2012

Neurobiology of Aging

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“…As discussed above, deregulated cytokine expression and unique aspects of gingival fibroblast metabolism are all likely to be important contributing factors in gingival overgrowth and development of highly synthetic or proliferative fibroblast phenotypes (Schmitt-Graff et al, 1994;Vaughan et al, 2000). In addition, a reduced rate of apoptosis is reported to contribute to the accumulation of gingival fibroblasts (Fujimori et al, 2001), perhaps with a greater synthetic or proliferative phenotype in nifedipine-induced gingival overgrowth (Kessler et al, 2001;Schild and Trueb, 2002), though this is a novel and understudied area at this time.…”

Section: Fibroblast Subpopulations and Fibroblast Differentiationmentioning

confidence: 98%

Connective Tissue Metabolism and Gingival Overgrowth

Trackman

Kantarcı

2004

Critical Reviews in Oral Biology & Medicine

135

152

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Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.

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“…An interesting in vitro study of the effect of nifedipine on gingival fibroblasts in the presence or absence of the macrophagelike cell line RAW264 cells revealed that LPS stimulation of iNOS was inhibited by nifedipine and could mediate the nifedipine inhibition of apoptosis (Fujimori et al 2001). Whether this effect of nifedipine occurs in vivo or with primary human macrophages has yet to be determined, but could be a contributing mechanism of the inhibited apoptosis in nifedipineinduced gingival overgrowth observed in human gingiva (Kantarci et al 2007).…”

Section: Are All Drug-induced Forms Of Gingival Overgrowth Fibrotic?mentioning

confidence: 99%

Molecular and Clinical Aspects of Drug-induced Gingival Overgrowth

Trackman

Kantarcı²

2015

J Dent Res

125

109

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Drug-induced gingival overgrowth is a tissue-specific condition and is estimated to affect approximately one million North Americans. Lesions occur principally as side-effects from phenytoin, nifedipine, or ciclosporin therapy in approximately half of the people who take these agents. Due to new indications for these drugs, their use continues to grow. Here, we review the molecular and cellular characteristics of human gingival overgrowth lesions and highlight how they differ considerably as a function of the causative drug. Analyses of molecular signaling pathways in cultured human gingival fibroblasts have provided evidence for their unique aspects compared with fibroblasts from the lung and kidney. These findings provide insights into both the basis for tissue specificity and into possible therapeutic opportunities which are reviewed here. Although ciclosporin-induced gingival overgrowth lesions exhibit principally the presence of inflammation and little fibrosis, nifedipine-and especially phenytoin-induced lesions are highly fibrotic. The increased expression of markers of gingival fibrosis, particularly CCN2 [also known as connective tissue growth factor (CTGF)], markers of epithelial to mesenchymal transition, and more recently periostin and members of the lysyl oxidase family of enzymes have been documented in phenytoin or nifedipine lesions. Some oral fibrotic conditions such as leukoplakia and oral submucous fibrosis, after subsequent additional genetic damage, can develop into oral cancer. Since many pathways are shared, the study of gingival fibrosis and comparisons with characteristics and molecular drivers of oral cancer would likely enhance understandings and functional roles of molecular drivers of these oral pathologies.

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Inhibition by nifedipine of adherence- and activated macrophage-induced death of human gingival fibroblasts

Cited by 27 publications

References 26 publications

Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model

Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model

Connective Tissue Metabolism and Gingival Overgrowth

Molecular and Clinical Aspects of Drug-induced Gingival Overgrowth

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