Lack of influence of cyclosporin A on levels of gingival procollagen types I and III mRNAs in rats of different ages

Redlich, Meir; Greenfeld, Ziv; Cooperman, Helena; Pisanty, Sara; Shoshan, S.

doi:10.1016/s0003-9969(97)00015-0

Cited by 6 publications

(3 citation statements)

References 33 publications

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“…Redlich et al . (28) demonstrated that the administration of cyclosporin A to rats did not change the levels of mRNAs for both procollagen types I and III in the gingiva of either young or old rats. Therefore, age did not influence collagen and non‐collagenous protein synthesis in the gingiva of cyclosporin A treated rats.…”

Section: Discussionmentioning

confidence: 99%

Combined effects of cyclosporin and nifedipine on gingival overgrowth in rats is not age dependent

Spolidório¹,

Spolidorio²,

C³

et al. 2003

J of Periodontal Research

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Section: Discussionmentioning

confidence: 99%

Combined effects of cyclosporin and nifedipine on gingival overgrowth in rats is not age dependent

Spolidório¹,

Spolidorio²,

C³

et al. 2003

J of Periodontal Research

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“…While cyclosporin A was found to increase glycosaminoglycan secretion by fibroblasts (Newell and Irwin, 1997), and nifedipine and phenytoin increased heparan levels (Saito et al, 1996), other studies failed to report any differences in vivo (Romanos et al, 1992(Romanos et al, , 1993Rocha et al, 2000;Martins et al, 2003). Several studies demonstrate that these drugs inhibit gingival fibroblast extracellular matrix production and/or cell proliferation in vitro (Modéer et al, 1982Salo et al, 1990;Stabellini et al, 1991;McKevitt and Irwin, 1995;Redlich et al, 1997). These findings are inconsistent with the in vivo characteristics of drug-induced gingival overgrowth.…”

Section: Direct Effects Of Phenytoin Cyclosporin and Nifedipine On mentioning

confidence: 99%

Connective Tissue Metabolism and Gingival Overgrowth

Trackman

Kantarcı

2004

Critical Reviews in Oral Biology & Medicine

136

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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“…The abundant synthesis of collagen in these tissues is balanced by an equally rapid rate of intracellular degradation (9), a process that is mediated by the phagocytic pathway in fibroblasts (10). In CsA-induced gingival overgrowth, there is a net increase in collagen (11), but CsA does not increase collagen expression (12) and does not substantially alter collagenase levels (13). Instead, the net increase in collagen is apparently due to reduced phagocytosis by fibroblasts (11).…”

mentioning

confidence: 99%

Mechanism of Cyclosporin-induced Inhibition of Intracellular Collagen Degradation

Arora

Silvestri

Ganß

et al. 2001

Journal of Biological Chemistry

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The immunosuppressant cyclosporin A (CsA) markedly inhibits collagen degradation by an intracellular phagocytic pathway in fibroblasts, an effect that can lead to massive gingival overgrowth. We used a collagen bead model of collagen phagocytosis to determine whether CsA inhibits internalization by blocking efflux of calcium from endoplasmic reticulum (ER) and mitochondrial calcium stores. CsA caused dose-dependent inhibition of phagocytosis of collagen-coated (but not bovine serum albumin-coated) beads. Chelation of intracellular Ca 2؉ with BAPTA/AM or inhibition of Ca 2؉ -ATPase of ER stores with thapsigargin reduced collagen bead phagocytosis. Measurement of intracellular calcium by ratio fluorometry showed increases in response to collagen-coated beads. Preincubation with CsA or thapsigargin caused a >3-fold decrease in intracellular calcium elevations in response to stimulation with collagen beads. Direct measurements of Ca 2؉ in mitochondrial and ER stores showed that CsA only slightly inhibited collagen bead-induced discharge of calcium from mitochondria, but almost completely blocked discharge from ER stores. We reduced the numbers of mitochondria with chronic ethidium bromide treatment to test for the importance of ER/mitochondrial interactions. In these cells, CsA delayed collagen bead-induced calcium discharge from mitochondria. Collectively, these data indicate that CsA inhibits collagen phagocytosis by blocking calcium release from ER stores and may perturb functional interactions between the ER and mitochondria that regulate calcium stores.

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Lack of influence of cyclosporin A on levels of gingival procollagen types I and III mRNAs in rats of different ages

Cited by 6 publications

References 33 publications

Combined effects of cyclosporin and nifedipine on gingival overgrowth in rats is not age dependent

Combined effects of cyclosporin and nifedipine on gingival overgrowth in rats is not age dependent

Connective Tissue Metabolism and Gingival Overgrowth

Mechanism of Cyclosporin-induced Inhibition of Intracellular Collagen Degradation

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