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丝裂原活化蛋白激酶激活的蛋白激酶2基因敲除小鼠中恶唑酮诱导的皮肤炎症减轻。

Reduced oxazolone-induced skin inflammation in MAPKAP kinase 2 knockout mice.

作者信息

Funding Anne T, Johansen Claus, Gaestel Matthias, Bibby Bo M, Lilleholt Louise L, Kragballe Knud, Iversen Lars

机构信息

Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark.

出版信息

J Invest Dermatol. 2009 Apr;129(4):891-8. doi: 10.1038/jid.2008.322. Epub 2008 Nov 6.

Abstract

Mitogen-activated protein kinase (MAPK) AP kinase 2 (MK2) is a serine/threonine kinase that is phosphorylated and activated by p38 MAPK. MK2 regulates the expression of various proinflammatory cytokines including TNF-alpha, IL-1beta, IL-6, and IL-8. Recently, MK2 was demonstrated to be activated in lesional psoriatic epidermis. This study investigates for the first time the role of MK2 in skin inflammation using the model of oxazolone-induced acute allergic contact dermatitis in mice. We show that oxazolone treatment leads to increased expression and sustained activation of both p38 MAPK and MK2. The inflammatory response was determined by ear thickness, myeloperoxidase activity, and histology after oxazolone challenge. Pretreatment with the p38 MAPK inhibitor SB202190 and genetic ablation of MK2 inhibit this inflammatory response. In particular, IL-1beta and, to a smaller but significant extent, also TNF-alpha and IFN-gamma expression were decreased in MK2 knockout mice compared with wild-type mice. These results indicate that MK2 is a potential target for the treatment of inflammatory skin diseases.

摘要

丝裂原活化蛋白激酶(MAPK)AP激酶2(MK2)是一种丝氨酸/苏氨酸激酶,可被p38 MAPK磷酸化并激活。MK2调节多种促炎细胞因子的表达,包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和白细胞介素-8(IL-8)。最近,研究发现MK2在银屑病皮损表皮中被激活。本研究首次使用恶唑酮诱导的小鼠急性过敏性接触性皮炎模型,探讨MK2在皮肤炎症中的作用。我们发现,恶唑酮处理可导致p38 MAPK和MK2的表达增加及持续激活。通过测量恶唑酮激发后的耳厚度、髓过氧化物酶活性和组织学来确定炎症反应。用p38 MAPK抑制剂SB202190预处理和MK2基因敲除可抑制这种炎症反应。特别是,与野生型小鼠相比,MK2基因敲除小鼠中IL-1β的表达降低,TNF-α和干扰素-γ(IFN-γ)的表达也有较小但显著的降低。这些结果表明,MK2是治疗炎症性皮肤病的一个潜在靶点。

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