CCR4 and CCR10 are expressed on epidermal keratinocytes and are involved in cutaneous immune reaction

Fujimoto, Seiki; Uratsuji, Hideya; Saeki, Hidehisa; Kagami, Shinji; Tsunemi, Yuichiro; Komine, Mayumi; Tamaki, Kunihiko

doi:10.1016/j.cyto.2008.07.472

Cited by 30 publications

(22 citation statements)

References 28 publications

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“…Collectively, TARC/CCL17 and its receptor CCR4 can be a major chemokine and chemokine receptor in the pathogenesis of atopic dermatitis (Soler et al, 2003). MDC/CCL22 is a Th2 type chemokine, which is another important chemoattractant for lymphocytes infiltration in inflammatory sites, and its receptor is CCR4 as TARC (Soler et al, 2003;Fujimoto et al, 2008). Recent report demonstrated that MDC/ CCL22 is expressed in HaCaT cells when the cells are stimulated with IFN-γ and TNF-α (Xiao et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

Choi

Lee

et al. 2010

Arch. Pharm. Res.

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We recently reported the inhibitory effect of an oral administration of a Sophora flavescens Aiton methanol extract on the development of atopic dermatitis in the NC/Nga model mice. Heme oxygenase (HO)-1 has recently emerged as an important cytoprotective enzyme against oxidative stress and inflammatory responses in many cell types. The aim of this study was to investigate the possible mechanism by which prenylated chalcone (PC, 7,9,2',4'-tetrahydroxy-8-isopentenyl-5-methoxychalcone), a natural product isolated from S. flavescens, inhibited cytokine-induced Th2 chemokine expression in human keratinocytes, HaCaT cells. The level of chemokine expression was measured by reverse transcription-polymerase chain reaction and HO-1 study was performed by Western blot analysis. Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha)-induced thymus- and activation-regulated chemokine (TARC/CCL17), macrophage-derived chemokine (MDC/CCL22), cutaneous T-cell attracting chemokine (CTACK/CCL27) expression in a dose-dependent manner. Interestingly, PC significantly suppressed IFN-gamma and TNF-alpha-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression via the induction of heme oxygenase (HO)-1. This suppression was completely restored by HO-1 siRNA, suggesting a direct role of HO-1 for the suppressive effect. Furthermore, exogenous CO, but not other end products of HO-1 activity, also suppressed IFN-gamma and TNF-alpha-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression. These results demonstrate that prenylated chalcone induces HO-1 expression, which in turn HO-1 and/or CO suppresses Th2 chemokine expressions induced by cytokines in human HaCaT cells.

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Section: Discussionmentioning

confidence: 99%

Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

Choi

Lee

et al. 2010

Arch. Pharm. Res.

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“…97 Several other ligand-receptor combinations appear to positively influence keratinocyte migration and proliferation in vitro. 98,99 In vivo studies in CXCL11…”

Section: Remodeling Phasementioning

confidence: 99%

Chemokines in Wound Healing and as Potential Therapeutic Targets for Reducing Cutaneous Scarring

Rees¹,

Greaves²,

Baguneid

et al. 2015

Advances in Wound Care

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“…Primers for amplification, and the sizes of respective PCR products were as follows: AdipoR1, 59-AATTCCTGAGCGCTTCTTTCCT-39 and 59-CAT-AGAAGTGGACAAAGGCTGC-39; AdipoR2, 59-TGCAGCCATTAT-AGTCTCCCAG-39 and 59-GAATGATTCCACTCAGGCCTAG-39 (25); calreticulin, 59-AAGTTCTACGGTGACGAGGAG-39 and 59-GTCGA-TGTTCTGCTCATGTTC-39 (26); T-cadherin, 59-GCCACGATCATGAT-CGATGAC-39 and 59-GTCTTCATTTTCCACTTTGA-39 (27); and glyceraldehyde-3-phosphate dehydrogenase gene, 59-TGAAGGTCGGAGTCA-ACGGATTTGGT-39 and 59-CATGTGGGCCATGAGGTCCACCAC-39 (28). PCR was performed by 94˚C for 5 min, 30 cycles of 94˚C for 45 s, 60˚C for 45 s, and 72˚C for 45 s and a final extension at 72˚C for 3 min.…”

Section: Rt-pcr and Quantitative Real-time Rt-pcr Analysismentioning

confidence: 99%

Adiponectin Regulates Cutaneous Wound Healing by Promoting Keratinocyte Proliferation and Migration via the ERK Signaling Pathway

Shibata

Tada

Asano

et al. 2012

The Journal of Immunology

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135

109

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Diabetic patients are at high risk of developing delayed cutaneous wound healing. Adiponectin plays a pivotal role in the pathogenesis of diabetes and is considered to be involved in various pathological conditions associated with diabetes; however, its role in wound repair is unknown. In this study, we elucidated the involvement of adiponectin in cutaneous wound healing in vitro and in vivo. Normal human keratinocytes expressed adiponectin receptors, and adiponectin enhanced proliferation and migration of keratinocytes in vitro. This proliferative and migratory effect of adiponectin was mediated via AdipoR1/AdipoR2 and the ERK signaling pathway. Consistent with in vitro results, wound closure was significantly delayed in adiponectin-deficient mice compared with wild-type mice, and more importantly, keratinocyte proliferation and migration during wound repair were also impaired in adiponectin-deficient mice. Furthermore, both systemic and topical administration of adiponectin ameliorated impaired wound healing in adiponectin-deficient and diabetic db/db mice, respectively. Collectively, these results indicate that adiponectin is a potent mediator in the regulation of cutaneous wound healing. We propose that upregulation of systemic and/or local adiponectin levels is a potential and very promising therapeutic approach for dealing with diabetic wounds.

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CCR4 and CCR10 are expressed on epidermal keratinocytes and are involved in cutaneous immune reaction

Cited by 30 publications

References 28 publications

Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

Chemokines in Wound Healing and as Potential Therapeutic Targets for Reducing Cutaneous Scarring

Adiponectin Regulates Cutaneous Wound Healing by Promoting Keratinocyte Proliferation and Migration via the ERK Signaling Pathway

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