PPARβ/δ在角质形成细胞对炎症反应中的关键作用。
Critical roles of PPAR beta/delta in keratinocyte response to inflammation.
作者信息
Tan N S, Michalik L, Noy N, Yasmin R, Pacot C, Heim M, Flühmann B, Desvergne B, Wahli W
机构信息
Institut de Biologie Animale, Université de Lausanne, CH-1015 Lausanne, Switzerland.
出版信息
Genes Dev. 2001 Dec 15;15(24):3263-77. doi: 10.1101/gad.207501.
Abstract
The immediate response to skin injury is the release of inflammatory signals. It is shown here, by use of cultures of primary keratinocytes from wild-type and PPAR beta/delta(-/-) mice, that such signals including TNF-alpha and IFN-gamma, induce keratinocyte differentiation. This cytokine-dependent cell differentiation pathway requires up-regulation of the PPAR beta/delta gene via the stress-associated kinase cascade, which targets an AP-1 site in the PPAR beta/delta promoter. In addition, the pro-inflammatory cytokines also initiate the production of endogenous PPAR beta/delta ligands, which are essential for PPAR beta/delta activation and action. Activated PPAR beta/delta regulates the expression of genes associated with apoptosis resulting in an increased resistance of cultured keratinocytes to cell death. This effect is also observed in vivo during wound healing after an injury, as shown in dorsal skin of PPAR beta/delta(+/+) and PPAR beta/delta(+/-) mice.
摘要
皮肤损伤的即时反应是炎症信号的释放。通过使用来自野生型和PPARβ/δ（-/-）小鼠的原代角质形成细胞培养物表明，包括TNF-α和IFN-γ在内的此类信号可诱导角质形成细胞分化。这种细胞因子依赖性细胞分化途径需要通过应激相关激酶级联反应上调PPARβ/δ基因，该激酶级联反应靶向PPARβ/δ启动子中的AP-1位点。此外，促炎细胞因子还启动内源性PPARβ/δ配体的产生，这些配体对于PPARβ/δ的激活和作用至关重要。活化的PPARβ/δ调节与细胞凋亡相关的基因表达，导致培养的角质形成细胞对细胞死亡的抵抗力增强。在损伤后的伤口愈合过程中，在体内也观察到了这种效应，如在PPARβ/δ（+/+）和PPARβ/δ（+/-）小鼠的背部皮肤中所示。
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