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衰老和习惯性阳光照射对培养的人角质形成细胞对模拟太阳辐射的基因反应的影响。

Effect of aging and habitual sun exposure on the genetic response of cultured human keratinocytes to solar-simulated irradiation.

作者信息

Garmyn M, Yaar M, Boileau N, Backendorf C, Gilchrest B A

机构信息

USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts.

出版信息

J Invest Dermatol. 1992 Dec;99(6):743-8. doi: 10.1111/1523-1747.ep12614470.

Abstract

Aging and chronic sun exposure are known to be associated with decreased cutaneous immune function, changes in the balance between epidermal proliferation and differentiation, and a greatly enhanced risk of photocarcinogenesis. However, their specific effects on the response of human keratinocytes to ultraviolet (UV) irradiation are unknown. We therefore asked whether aging and photoaging modulate the response at the mRNA level to UV-inducible genes implicated in immunomodulation and/or growth control. Cultured human keratinocytes derived from newborn, young adult, and old adult donors were exposed to a single physiologic dose of solar-simulated UV or sham irradiation and harvested at 1, 4, 8, 24, and 48 h post-irradiation for northern blot analysis. Specific mRNA was detected using cDNA probes encoding the proto-oncogenes c-fos and c-myc and the growth-arrest and DNA damage (GADD153) gene, all recently shown by our laboratory to be modulated by UV in newborn keratinocytes; interleukin (IL)-1a, IL-1b, and the IL-1 receptor antagonist (IL-1ra), two keratinocyte cytokines and their competitive inhibitor, implicated in the immunomodulatory effect of UV; and SPR2, a recently cloned gene known to be induced during normal keratinocyte differentiation and by lethal UV-C irradiation. Our data suggest that aging alone strikingly increases the baseline expression of SPR2 and IL-1ra but has relatively little effect on the response to UV for the other genes examined. In contrast, the combination of aging and habitual sun exposure, so-called photoaging, markedly increases c-fos inducibility and decreases baseline expression of SPR2 and IL-1ra relative to that in cells from sun-protected skin of the same donors. The implied alterations in signal transduction and differentiation state observed in cells derived from habitually sun-exposed sites of old adults may explain in part the predisposition to photocarcinogenesis in photoaged skin.

摘要

已知衰老和长期日晒与皮肤免疫功能下降、表皮增殖与分化平衡的改变以及光致癌风险的大幅增加有关。然而,它们对人类角质形成细胞对紫外线(UV)照射反应的具体影响尚不清楚。因此,我们研究衰老和光老化是否在mRNA水平上调节与免疫调节和/或生长控制相关的紫外线诱导基因的反应。将来自新生儿、年轻成年人和老年人供体的培养人类角质形成细胞暴露于单一生理剂量的模拟太阳紫外线或假照射,并在照射后1、4、8、24和48小时收获,用于Northern印迹分析。使用编码原癌基因c-fos和c-myc以及生长停滞和DNA损伤(GADD153)基因的cDNA探针检测特定mRNA,我们实验室最近发现这些基因在新生儿角质形成细胞中受紫外线调节;白细胞介素(IL)-1α、IL-1β和IL-1受体拮抗剂(IL-1ra),两种角质形成细胞细胞因子及其竞争性抑制剂,与紫外线的免疫调节作用有关;以及SPR2,一个最近克隆的基因,已知在正常角质形成细胞分化过程中以及致死性紫外线-C照射时被诱导。我们的数据表明,仅衰老就显著增加SPR2和IL-1ra的基线表达,但对所检测的其他基因对紫外线的反应影响相对较小。相比之下,衰老与长期日晒相结合,即所谓的光老化,相对于来自同一供体防晒皮肤的细胞,显著增加c-fos的诱导性,并降低SPR2和IL-1ra的基线表达。在老年人长期日晒部位的细胞中观察到的信号转导和分化状态的潜在改变可能部分解释了光老化皮肤中光致癌的易感性。

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