β-carotene inhibits UVA-induced matrix metalloprotease 1 and 10 expression in keratinocytes by a singlet oxygen-dependent mechanism

Wertz, Karin; Seifert, Nicole; Hunziker, Petra Buchwald; Riss, Georges; Wyss, Adrian; Lankin, Christopher; Góralczyk, Regina

doi:10.1016/j.freeradbiomed.2004.05.018

Cited by 45 publications

(28 citation statements)

References 104 publications

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“…Consistent with our observations, ROS are known to mediate low-dose UVB-induced MMP expression (Brenneisen et al, 2002;Vayalil et al, 2004;Wertz et al, 2004). In particular, the importance of ROS in photo-aging is underlined by extensive evidence that exposure to antioxidants decreases UVB-induced MMP expression in dermal skin cells (Kang et al, 2003;Vayalil et al, 2004;Wertz et al, 2004;Zaid et al, 2007). However, neither the source of ROS generated in response to low-dose UVB irradiation nor the pathway by which they are generated in the skin has been clearly understood.…”

Section: Discussionsupporting

confidence: 92%

“…This conclusion is based on the following observations: (1) BLT2 blockage using a specific antagonist or siRNA reduces low-dose UVB irradiation-induced MMP-1 expression; (2) BLT2 overexpression in HaCaT cells is sufficient to cause significant up-regulation of MMP-1 expression; (3) levels of both BLT2 ligands (LTB 4 and 12(S)-HETE) and the synthesizing enzymes for those ligands (5-LO and 12-LO, respectively) are considerably increased in response to UVB irradiation in HaCaT cells; and (4) Additionally, we provide evidence suggesting that BLT2-mediated MMP-1 upregulation occurs through a signaling pathway dependent on ROS production and the subsequent stimulation of ERK. Consistent with our observations, ROS are known to mediate low-dose UVB-induced MMP expression (Brenneisen et al, 2002;Vayalil et al, 2004;Wertz et al, 2004). In particular, the importance of ROS in photo-aging is underlined by extensive evidence that exposure to antioxidants decreases UVB-induced MMP expression in dermal skin cells (Kang et al, 2003;Vayalil et al, 2004;Wertz et al, 2004;Zaid et al, 2007).…”

Section: Discussionsupporting

confidence: 88%

“…To test this hypothesis, we determined whether ERK phosphorylation is affected by pretreatment with the antioxidant DPI or by BLT2 knockdown with siBLT2. In agreement with previous observations reporting that mitogen-activated protein kinases (MAPKs), including ERK, play roles in UV-induced MMP-1 expression (Brenneisen et al, 2002;Wertz et al, 2004;Shin et al, 2008;Shim et al, 2009;Yang et al, 2009), ERK phosphorylation was greatly enhanced by low-dose UVB irradiation in HaCaT cells ( Figure 5A). Additionally, JNK and p38 kinase levels were also stimulated by UVB irradiation, although the levels of phosphorylation were not as great as those of ERK.…”

Section: Erk Phosphorylation Lies Downstream Of the Blt2-ros Cascade supporting

confidence: 93%

“…We found that low-dose UVB irradiation significantly upregulated MMP-1 expression in human keratinocyte HaCaT cells through a pathway dependent on BLT2 (a receptor for LTB 4 and 12(S)-HETE). We also demonstrated that in UVB-irradiated HaCaT cells, BLT2 mediates MMP-1 upregulation through a signaling pathway dependent on reactive oxygen species (ROS) production and the subsequent stimulation of extracellularregulated kinase (ERK), two well-characterized mediators of UVB-induced MMP-1 expression (Whitmarsh and Davis, 1996;Wertz et al, 2004;Kim et al, 2005;Shin et al, 2008;Yang et al, 2009). In agreement with the proposed role of BLT2 as a mediator of UVB-induced MMP-1 expression, we observed that BLT2 overexpression markedly enhanced MMP-1 expression and ERK phosphorylation.…”

Section: Introductionmentioning

confidence: 82%

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Low-dose UVB irradiation stimulates matrix metalloproteinase-1 expressionviaa BLT2-linked pathway in HaCaT cells

2010

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Section: Erk Phosphorylation Lies Downstream Of the Blt2-ros Cascade supporting

confidence: 93%

Section: Introductionmentioning

confidence: 82%

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Low-dose UVB irradiation stimulates matrix metalloproteinase-1 expressionviaa BLT2-linked pathway in HaCaT cells

2010

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“…To investigate the functional effects of increased TGF-β/Smad activation on RA pathway, the MMCs were co-transiently transfected with Smad2/3 expression vectors and the reporter construct pGL3(RARE)5-tk-luc (RARE-tk-Luc), which contains five DR5-type RAREs from the human RARβ promoter and responds well to RA induction [21]. As shown in Fig.…”

Section: Activation Of Tgf-β/smad Signaling Suppressed Rar-mediated Gmentioning

confidence: 99%

Negative Functional Interaction of Retinoic Acid and TGF-β Signaling Mediated by TG-interacting Factor During Chondrogenesis

Zhang

Li²,

Tang³

et al. 2009

Cell Physiol Biochem

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We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-β/Smad signaling. However, the molecular link between RA and TGF-β signaling is unknown. Using a mouse embryo palate mesenchyme micomass cultures (MMCs) system, we explored interactions of RA and TGF-β signaling during chondrogenesis. We found that atRA suppressed chondrogenesis and Smad2/3 phosphorylation regardless of the presence of TGF-β3. Functional assays indicated that TGF-β3 treatment or co-transfection of expressing Smad2/3 vectors suppressed atRA-induced RARE-tk-Luc activity. Conversely, atRA or RAR-overexpression repressed TGF-β3-induced transactivation of the TGF-β-responsive reporter, p3TP-Lux. ChIP assay revealed the binding of the Smad transcriptional co-repressor TGIF (TG-interacting factor, TGIF) to RARβ promoter in control MMCs, but this association was decreased by the addition of RA and increased by TGF-β3, respectively. Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-β signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-β3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-β3 to relieve atRA-mediated the suppression of chondrogenesis. Furthermore, we demonstrated that the effects of atRA on TGF-β-dependent gene activation and of TGF-β on RA-dependent gene activation are mediated by TGIF with siRNA to downregulate TGIF. Collectively, these findings indicated a negative functional interplay of RA and TGF-β signaling mediated by TGIF to modulate chondrogenesis in MMCs.

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Inhibition of UV‐induced matrix metabolism by a myristoyl tetrapeptide

Kwon

Ahn

Kim

et al. 2015

Cell Biology International

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Regulation of extracellular matrix (ECM) composition is important in tissue homeostasis and function. We screened small peptides for their ability to inhibit ultraviolet (UV)-induced cell metabolism in epidermal fibroblasts. We found that UV irradiation increased matrix metalloproteinase (MMP) expression and inflammatory gene expression in human Hs68 fibroblast cells. We also demonstrated that a myristoyl tetrapeptide with the amino acid sequence Gly-Leu-Phe-Trp (mGLFW) suppressed the UV-induced expression of MMPs and inflammatory genes. Moreover, mGLFW stimulated the expression of ECM proteins in Hs68 fibroblasts. In order to provide the mechanism of action for mGLFW, we investigated UV-induced signaling changes in the presence of mGLFW using a cDNA microarray. UV exposure increased the expression of MMP genes, such as MMP1, MMP3, and MMP14, and inflammation-related genes, including interleukin 1 receptor and peroxisome proliferator-activated receptor gamma (PPARγ). Treatment with mGLFW abrogated the UV-induced expression of MMP-related genes and inflammatory genes. In addition, mGLFW increased the expression of collagen genes, including COL1A1, COL1A2, and COL5A1. We examined whether the activation of AP-1, a UV-activated transcription factor, is suppressed by mGLFW. The results demonstrated that AP-1 expression increased upon UV exposure and that this expression was inhibited by mGLFW. In conclusion, our results demonstrate that mGLFW reversed the effects of UV exposure by enhancing the expression of collagen proteins and suppressing the expression of MMPs, which degrade the ECM.

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β-carotene inhibits UVA-induced matrix metalloprotease 1 and 10 expression in keratinocytes by a singlet oxygen-dependent mechanism

Cited by 45 publications

References 104 publications

Low-dose UVB irradiation stimulates matrix metalloproteinase-1 expressionviaa BLT2-linked pathway in HaCaT cells

Low-dose UVB irradiation stimulates matrix metalloproteinase-1 expressionviaa BLT2-linked pathway in HaCaT cells

Negative Functional Interaction of Retinoic Acid and TGF-β Signaling Mediated by TG-interacting Factor During Chondrogenesis

Inhibition of UV‐induced matrix metabolism by a myristoyl tetrapeptide

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