Sphingosylphosphorylcholine down-regulates filaggrin gene transcription through NOX5-based NADPH oxidase and cyclooxygenase-2 in human keratinocytes

Choi, Hyun Jung; Kim, Shinhyoung; Kim, Hyoung-June; Kim, Kwang-Mi; Lee, Chang‐Hoon; Shin, Jennifer Hyunjong; Noh, Minsoo

doi:10.1016/j.bcp.2010.03.009

Cited by 24 publications

(21 citation statements)

References 54 publications

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“…30) SPc downregulates filaggrin gene transcription, which also leads to skin dryness and the disruption of the skin barrier. 31) SPc is also increased in the lesional epidermis of mice with chronic allergic dermatitis. 32) Intradermal injection of SPc, but not of sphingomyelin and sphingosine, elicits scratching in mice.…”

Section: Lipid Mediatorsmentioning

confidence: 90%

Potential New Therapeutic Targets for Pathological Pruritus

Kuraishi

2013

Biological & Pharmaceutical Bulletin

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Very few approved medications are indicated for the treatment of pruritus, and drug development for pruritic diseases is awaited. During the past two decades, progress has been made in understanding the molecular basis of the physiology and pathophysiology of pruritus. Newly identified potential targets for pathological pruritus include receptors (histamine H 4 receptor, leukotriene B 4 receptors, interleukin-31 receptor A, bombesin BB 2 receptor, toll-like receptor 3, α-adrenoceptor, and opioid μ-and κ-receptors), channels (transient receptor potential (TRP) V3 and TRPA1 channels), and enzymes (histidine decarboxylase, sphingomyelin glucosylceramide deacylase, 5-lipoxygenase, leukotriene A 4 hydrolase, and autotaxin). The development of specific, effective blockers and agonists/antagonists of these targets is awaited.

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Section: Lipid Mediatorsmentioning

confidence: 90%

Potential New Therapeutic Targets for Pathological Pruritus

Kuraishi

2013

Biological & Pharmaceutical Bulletin

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“…Our continuing efforts of finding pruritogens showed that 12(S)-HPETE and sphingosylphosphorylcholine (SPC) induced itch-scratch response in mice. Recently it is reported that SPC downregulates the expression of filaggrin (Choi et al, 2010). Therefore, SPC or Gsp is not any more simple byproducts of abnormal skin barrier but they can act as main factors affecting symptoms of atopic dermatitis such as itching and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Kim¹,

Kim²,

Noh³

et al. 2010

Biomolecules and Therapeutics

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-Pruritus is one of major symptoms in atopic dermatis. The pathophysiological mechanism of pruritus is unclear. The search for pruritogen is important in elucidating the pathophysiological mechanism of pruritus in atopic dermatitis. Glucosylsphingosine (Gsp) is upregulated in the strateum corneum of atopic dermatitis patients. We investigated to determine whether Gsp induces itch-scratch responses (ISRs) in mice. Intradermal administration of Gsp induces ISRs. Gsp dose-dependently induced scratching response at 50-500 nmol/site range. Pretreatment with naltrexone, an opioid μ receptor antagonist, and capsaicin, a TrpV1 receptor agonist, inhibited Gsp-induced ISRs. Additionally, Gsp-induced ISRs were also suppressed by cyproheptadine, an antagonist of serotonin receptor. These findings suggest that Gsp-induced scratching might be at least partly mediated by capsaicin-sensitive primary afferents, and the opioids receptor systems might be involved in transmission of itch signaling in the central nervous system. Furthermore, our findings suggest that Gsp-induced ISRs may be attributable to the serotonin-mediated pathways and Gsp is not any more one of byproducts of abnormal skin barrier but can lead to induce pruritus, one of typical symptoms of atopic dermatitis.

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“…Primary NHKs from neonatal foreskin were purchased from Lonza (Basel, Switzerland) and cultured as previously reported (Choi et al, 2010). NHK cells were grown to 100% confluence, and then cell culture medium was exchanged for keratinocyte basal medium (KBM, Lonza) supplemented with hEGF (KGM-2 BulletKit, Lonza) for 24 h. NHK cells, conditioned with the KBM medium with hEGF, were stimulated with recombinant human interleukin (IL)-1α (R&D systems, Minneapolis, MN, USA), tumor necrosis factor α (TNFα, R&D systems), IL-4 (R&D systems), IL-6 (R&D systems), IL-17A (Sigma Aldrich, St.…”

Section: Methodsmentioning

confidence: 99%