Retinoid modulation of connective tissue metabolism in keloid fibroblast cultures

Abergel, R. P.

doi:10.1001/archderm.121.5.632

Cited by 21 publications

(6 citation statements)

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“…Daly et al (38) demonstrated that tretinoin significantly reduces collagen production of human primary cultured fibroblasts. Abergel et al (39) reported that tretinoin and isotretinoin significantly inhibit degradation activity of type I collagen fibers in keloid-derived fibroblasts. On the other hand, in the field of cancer cell study, degradation of type I and type IV collagen, and invasion into collagen matrix was reported to be significantly inhibited by retinoids (28).…”

Section: A B Cmentioning

confidence: 99%

Tretinoin reverses upregulation of matrix metalloproteinase‐13 in human keloid‐derived fibroblasts

Uchida

Yoshimura

Kitano

et al. 2003

Experimental Dermatology

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Keloids are skin abnormalities that are characterized by excessive deposition of collagen bundles in the dermis. Patients with keloids complain not only about their cosmetic appearance, but also about continuous itching and/or tenderness associated with chronic inflammation. Degradation of extracellular matrix (ECM) may be upregulated, associated with the expansion of keloids into circumferential skin, and high metabolic activity of keloid tissues may be due to increased matrix metalloproteinase (MMP) activity. Based on these hypotheses, we examined differences in expression of MMP-1, MMP-8, and MMP-13 between keloid-derived and normal dermal fibroblasts. Since retinoids are potent inhibitors of MMPs in the treatment of photoaged skin and cancers, we also examined whether or not tretinoin affects MMP expression of keloid-derived fibroblasts. The results of real-time polymerase chain reaction and ELISA demonstrated significant upregulation of MMP-13 and significant downregulation of MMP-1 and MMP-8 in keloid-derived fibroblasts, at both mRNA and protein levels. MMP-1 mRNA expression in the control group was significantly upregulated after the addition of tretinoin, whereas no significant change was observed in the keloid group. MMP-8 mRNA expression in the control group was significantly upregulated by tretinoin, with the peak at 12 h, while no significant change was observed in the keloid-derived fibroblasts. In contrast, the remarkably elevated MMP-13 mRNA expression in the keloid group was significantly suppressed, with the peak suppression at 12 h after addition of tretinoin, while MMP-13 mRNA expression in the control group was not significantly changed. The decrease in MMP-1 and MMP-8 may contribute to accumulation of type I and type III collagen in keloid tissues, and this mechanism may be modulated by molecular interaction with MMP-13. Tretinoin appeared to reverse the abnormal expression profile of MMPs in keloid-derived fibroblasts, such as markedly elevated expression of MMP-13, partly through inactivation of AP-1 pathway. The present results suggest that tretinoin may be clinically useful to improve the chronic inflammation seen in keloids and prevent expansion of keloid tissues into circumferential normal skin.

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Section: A B Cmentioning

confidence: 99%

Tretinoin reverses upregulation of matrix metalloproteinase‐13 in human keloid‐derived fibroblasts

Uchida

Yoshimura

Kitano

et al. 2003

Experimental Dermatology

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“…Several studies utilizing in vitro incubation systems have attested to the possibility that all-trans-retinoic acid and 13-cis-retinoic acid are potent inhibitors of connective tissue formation [120][121][122][123][124]. Specifically, these two retinoids have been shown to suppress collagen synthesis by cultured skin fibroblasts and this inhibition appears to occur on the pre-translational level [120,124].…”

Section: Pbarmacologic Inhibition Of Collagen Depositionmentioning

confidence: 99%

Extracellular Matrix of the Skin: 50 Years of Progress.

Uitto¹,

Olsen²,

Fazio³

1989

J Invest Dermatol

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The extracellular connective tissue matrix of the skin is a complex aggregate of distinct collagenous and non-collagenous components. Optimal quantities and delicate interactions of these components are necessary to maintain normal physiologic properties of skin. This overview summarizes the progress made in understanding the normal biology and biochemistry of the extracellular matrix, and will highlight cutaneous diseases with underlying molecular defects in the structure and expression of extracellular matrix components.

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“…However, because other teratogenic agents and conditions result in similar malformations, accentuation of cell death has also been proposed as a common teratogenic mechanism [3, 461. Mechanisms of teratogenesis other than these may be involved. Retinoids can both stimulate and inhibit cell growth [15,29,39,411, and it is well established that RAs profoundly influence differentiation (for reviews, see [39,531) and the metabolism of connective tissue extracellular matrix (ECM) [ 1,14,17,341. In addi-tion, the teratogenic effects of retinoids may be related to the proposed normal activity of retinoic acid as a signalling molecule during development.…”

Section: Introductionmentioning

confidence: 99%

Early heart development in the chick embryo: effects of isotretinoin on cell proliferation, α-actin synthesis, and development of contractions

et al. 1992

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Retinoid modulation of connective tissue metabolism in keloid fibroblast cultures

Cited by 21 publications

References 0 publications

Tretinoin reverses upregulation of matrix metalloproteinase‐13 in human keloid‐derived fibroblasts

Tretinoin reverses upregulation of matrix metalloproteinase‐13 in human keloid‐derived fibroblasts

Extracellular Matrix of the Skin: 50 Years of Progress.

Early heart development in the chick embryo: effects of isotretinoin on cell proliferation, α-actin synthesis, and development of contractions

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