Cellular and Molecular Mechanisms of Cutaneous Aging

Yaar, Mina; Gilchrest, Barbara A.

doi:10.1111/j.1524-4725.1990.tb01555.x

Cited by 80 publications

(40 citation statements)

References 48 publications

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“…Photoaging of skin is caused by genetically determined or intrinsic processes superimposed upon the degenerative changes due to solar radiation. 1) Alterations and deficiencies of collagen, the major structural component of skin, have been suggested to be a cause of the skin wrinkling observed in photoaged and naturally aged skin. 2,3) The dermis contains predominantly type I and type III collagen, elastin, proteoglycans, and fibronectin.…”

mentioning

confidence: 99%

Regulation Effect of 2',4',7-Trihydroxyisoflavone on the Expression of Matrix Metalloproteinase-1, 2 in Ultraviolet-B Irradiated Primary Cultured Old Aged Human Skin Fibroblasts

Moon

Kwak

Zee

et al. 2005

Biological & Pharmaceutical Bulletin

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Long term and repeated exposure of UV light on the skin often induces chronic skin diseases such as skin cancer as well as photoaging, and the mechanisms of these skin damages are closely associated with up-regulation of matrix metalloproteinase's (MMPs) activities. We investigated the effect of 2,4,7-trihydroxyisoflavone purified from the whole plants of Viola hondoensis W. BECKER et H BOISSIEU (Violaceae) on the expression of MMPs in UV-B irradiated old aged human skin fibroblasts. 2,4,7-trihydroxyisoflavone markedly reduced UV-induced MMP-1 expression, but not MMP-2, at the both mRNA and protein levels in a dose-dependent manner. Our report is the first description for the ability of 2,4,7-trihydroxyisoflavone to regulate MMP-1 expression from ultraviolet-B irradiated primary cultured old aged human skin fibroblasts.Key words Viola hondoensis; 2Ј,4Ј,7-trihydroxyisoflavone; matrix metalloproteinase (MMP)-1; MMP-2; aged human skin fibroblastThe skin aging process can be divided into intrinsic aging and photoaging. Damage to human skin due to repeated exposure to ultraviolet (UV) radiation (photoaging) and damage occurring as a result of the passage of time (intrinsic aging) are considered to be distinct entities rather than similar skin aging processes. Photoaging of skin is caused by genetically determined or intrinsic processes superimposed upon the degenerative changes due to solar radiation. 1) Alterations and deficiencies of collagen, the major structural component of skin, have been suggested to be a cause of the skin wrinkling observed in photoaged and naturally aged skin. 2,3)The dermis contains predominantly type I and type III collagen, elastin, proteoglycans, and fibronectin. Since collagen fibrils and elastin are responsible for the strength and resiliency of skin, their disarrangement during photoaging causes the skin to appear aged. Recently, it was suggested that excessive matrix degradation by UV-induced MMP-1 secreted by various cells, including, keratinocytes, fibroblasts, and inflammatory cells, contributes substantially to the connective tissue damage that occurs during photoaging. [4][5][6] The expression of MMPs proteins in the dermis of sunexposed and sun-protected skin of elderly subjects is known to differ. 5) Photodamaged skin of the elderly shows higher MMP-1 protein expression, than the intrinsically aged skin in the same individual.5) Thus, this resulting higher expression of MMP-1 in photoaged skin may cause severe collagen deficiency and wrinkling. Matrix metalloproteinases (MMPs) are a family of zinc-dependent endoproteinases that play pivotal roles in the dynamic remodeling of extracellular matrix. Based on substrate preference and structural homology, MMPs are sub-classified into functional groups: collagenases, gelatinases, stromelysins, matrilysins, membrane typeMMPs (MT-MMPs) and other non-classified MMPs. 7) MMPs are frequently overexpressed by the various extracellular stimuli including growth factors, cytokines, tumor promoters, and UV, and this increase in MMP-related ac...

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confidence: 99%

Regulation Effect of 2',4',7-Trihydroxyisoflavone on the Expression of Matrix Metalloproteinase-1, 2 in Ultraviolet-B Irradiated Primary Cultured Old Aged Human Skin Fibroblasts

Moon

Kwak

Zee

et al. 2005

Biological & Pharmaceutical Bulletin

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“…UVB-inducible genes comprise several proteinases, among them members of the matrixdegrading metalloproteinase (MMP) superfamily (9,16,(21)(22)(23). As to their proteolytic activity, various UVB-induced matrix-degrading metalloproteinases in dermal fibroblasts contribute to the breakdown of dermal interstitial collagen and other connective tissue components and, thus, besides initiating cutaneous photoaging (15,16,21,22,24) promote tumor invasion and metastasis (25,26).…”

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confidence: 99%

Activation of p70 Ribosomal Protein S6 Kinase Is an Essential Step in the DNA Damage-dependent Signaling Pathway Responsible for the Ultraviolet B-mediated Increase in Interstitial Collagenase (MMP-1) and Stromelysin-1 (MMP-3) Protein Levels in Human Dermal Fibroblasts

Brenneisen

Wenk

Wlaschek

et al. 2000

Journal of Biological Chemistry

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Ultraviolet B (UVB) irradiation has been shown to stimulate the expression of matrix-degrading metalloproteinases via generation of DNA damage and/or reactive oxygen species. Matrix-degrading metalloproteinases promote UVB-triggered detrimental long term effects like cancer formation and premature skin aging. Here, we were interested in identifying components of the signal transduction pathway that causally link UVBmediated DNA damage and induction of matrix-degrading metalloproteinase (MMP)-1/interstitial collagenase and MMP-3/stromelysin-1 in human dermal fibroblasts in vitro. The activity of p70 ribosomal S6 kinase, a downstream target of the FK506-binding protein-12/rapamycin-associated protein kinase (FRAP) kinase (RAFT1, mTOR), was identified to be 4.8 ؎ 0.8-fold, and MMP-1 and MMP-3 protein levels 2.4-and 11.5-fold increased upon UVB irradiation compared with mock-irradiated controls. The FRAP kinase inhibitor rapamycin and the DNA repair inhibitor aphidicolin significantly suppressed the UVB-mediated increase in p70 ribosomal S6 kinase activity by 50 -65% and MMP-1 and MMP-3 protein levels by 34 -68% and 42-88% compared with UVBirradiated fibroblasts. By contrast, the interleukin-1␤-mediated increase in MMP-1 and MMP-3 protein levels could not be suppressed by rapamycin. Collectively, our data suggest that the FRAP-controlled p70 ribosomal S6 kinase is an essential component of a DNA damagedependent, but not of the interleukin-1/cell membrane receptor-dependent signaling.In past years, two signaling pathways for the mammalian ultraviolet (UV) response have been identified. The first pathway comprises UV irradiation-dependent generation of reactive oxygen species near or within the cell membrane. UVgenerated reactive oxygen species activate receptor tyrosine kinases and protein kinases at the inner surface of the plasma membrane and elicit a signaling cascade, which activates transcription factors and the transcription of defined genes (1-3).The signaling cascade of the second pathway originates in the cell nucleus with indirect (oxidative) (4) or direct DNA damage as the primary signal, followed by passage of secondary "signals" to the cytoplasm, thereby activating specific signaling pathways, which eventually return to the nucleus and induce changes in transcription factors and gene expression (1,5,6).In view of the compelling evidence that the increase in ultraviolet-B (UVB) irradiation (280 -320 nm) on earth due to stratospheric ozone depletion represents a major environmental threat to the skin (7-9), we and others focused our studies on signaling cascades which mediate noxious UVB effects. UVB irradiation has recently been shown to generate lipid peroxides and hydroxyl radicals (HO ⅐ ) (10 -13) in skin cells with detrimental long term effects like cancer formation (9, 14) and premature aging (9, 15, 16). The major types of DNA lesions directly generated by UVB and artificial UVC irradiation predominantly occur at dipyrimidine sites with the formation of cyclobutane pyrimidine dimers (CPD) 1 and py...

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“…Cellular manifestations of intrinsic aging include decreased life span of cells, decreased responsiveness of cells to growth signals, which may reflect loss of cellular receptors to growth factors, and increased responsiveness to growth inhibitors. All these findings are more pronounced in cells derived from photodamaged skin [3].…”

Section: Introductionmentioning

confidence: 72%

Effects of Olibanum extracts on the collagenase activity and procollagen synthesis in Hs68 human fibroblasts and tyrosinase activity

Leem¹

2015

Advanced Science and Technology Letters

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Abstract. This study was designed to investigate the collagen metabolism and tyrosinase activity of Olibanum extracts (OE). The traditional effects are known to move blood, calm pain, solve oedema, and promote tissue regeneration. The effect of OE on type I procollagen production and collagenase (matrix metalloproteinase-1, henceforth referred as MMP-1) activity in human normal fibroblasts Hs68 after ultraviolet B (UVB, 312 nm) irradiation was measured by ELISA method. The tyrosinase activity after treatment of OE was measured as well. There was no cytotoxicity at all tested concentrations. The increased collagenase activity after UVB damage was significantly recovered by OE. The reduced type I procollagen production was not recovered by OE in UVB damaged Hs68 cells. OE did not reduce the tyrosinase activity and the L-DOPA oxidation. In conclusion, OE showed the anti-wrinkle effects via the collagenase inhibitory mechanism. Although more researches are needed to validate the efficacy, these results suggest that OE may have potential as an anti-aging ingredient in cosmetic herb markets.

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Cellular and Molecular Mechanisms of Cutaneous Aging

Cited by 80 publications

References 48 publications

Regulation Effect of 2',4',7-Trihydroxyisoflavone on the Expression of Matrix Metalloproteinase-1, 2 in Ultraviolet-B Irradiated Primary Cultured Old Aged Human Skin Fibroblasts

Regulation Effect of 2',4',7-Trihydroxyisoflavone on the Expression of Matrix Metalloproteinase-1, 2 in Ultraviolet-B Irradiated Primary Cultured Old Aged Human Skin Fibroblasts

Activation of p70 Ribosomal Protein S6 Kinase Is an Essential Step in the DNA Damage-dependent Signaling Pathway Responsible for the Ultraviolet B-mediated Increase in Interstitial Collagenase (MMP-1) and Stromelysin-1 (MMP-3) Protein Levels in Human Dermal Fibroblasts

Effects of Olibanum extracts on the collagenase activity and procollagen synthesis in Hs68 human fibroblasts and tyrosinase activity

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