Dermal damage promoted by repeated low-level UV-A1 exposure despite tanning response in human skin.
Dermal damage promoted by repeated low-level UV-A1 exposure despite tanning response in human skin.
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DOI：
10.1001/jamadermatol.2013.8417
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发表时间：
2014-04
期刊：
影响因子：
10.9
通讯作者：
Fisher, Gary J.
中科院分区：
文献类型：
--
作者：
Wang, Frank;Smith, Noah R.;Bao Anh Patrick Tran;Kang, Sewon;Voorhees, John J.;Fisher, Gary J.
太阳紫外线（UV）照射引起光老化，其特征在于为皮肤提供强度的I型胶原原纤维的断裂和减少的产生。UVB照射（280-320 nm）通过诱导基质金属蛋白酶（MMP）-1和抑制I型胶原合成引起这些变化。UVA照射（320-400 nm）在促进类似分子改变中的作用不太清楚，但值得考虑，因为它在自然日光中的丰度比UVB照射高10-100倍，并且比UVB照射更深地渗透到真皮中。大部分（约75%）的太阳UVA辐射由UVA 1辐射（340-400 nm）组成，这也是晒黑床的主要成分。评估日常生活中可能遇到的低水平UVA 1照射对MMP-1和I型前胶原（I型胶原的前体）表达的影响。正常人皮肤在UVA 1照射后的体内生化分析。学术推荐中心。无皮肤病的健康志愿者。通过色度计（色度计）在L* 变量（发光）下测量皮肤色素沉着，L * 变量的范围为0（黑色）至100（白色）。通过实时聚合酶链反应评估皮肤样品中的基因表达。将浅色人类皮肤（L*>65）暴露于低剂量（20 J/cm 2）的UVA 1照射多达四次（一次暴露/天），模拟来自持续约两小时的强烈阳光暴露的UVA水平。单次暴露于低剂量UVA 1照射使皮肤略微变暗，并且没有改变MMP-1或I型前胶原基因表达。通过重复低剂量UVA 1照射，皮肤会随着每次照射而逐渐变黑。尽管这种变暗，两个或两个以上的暴露于低剂量的UVA 1照射显着诱导MMP-1基因的表达，随着连续曝光逐步增加。重复的UVA 1照射并不能抑制I型前胶原的表达。有限数量的低剂量UVA 1暴露，如日常生活中常见的那样，可能通过影响胶原蛋白的分解而不是合成来促进光老化。轻度色素沉着个体反复低剂量UVA 1暴露后皮肤逐渐变黑并不能阻止UVA 1诱导的胶原溶解变化。因此，为了最佳地保护皮肤免受伤害，防晒配方应该过滤所有紫外线波长，包括UVA 1照射。
Solar ultraviolet (UV) irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin. UVB irradiation (280–320 nm) causes these changes by inducing matrix metalloproteinase (MMP)-1 and suppressing type I collagen synthesis. The role of UVA irradiation (320–400 nm) in promoting similar molecular alterations is less clear, yet important to consider, since it is 10–100 times more abundant in natural sunlight than UVB irradiation and penetrates deeper into the dermis than UVB irradiation. The majority (~75%) of solar UVA irradiation is comprised of UVA1 irradiation (340–400 nm), which is also the primary component of tanning beds. To evaluate the effects of low levels of UVA1 irradiation, as might be encountered in daily life, on expression of MMP-1 and type I procollagen (the precursor of type I collagen). In vivo biochemical analyses after UVA1 irradiation of normal human skin. Academic referral center. Healthy human volunteers without skin disease. Skin pigmentation was measured by a color meter (chromameter) under the L* variable (luminescence), which ranges from 0 (black) to 100 (white). Gene expression in skin samples was assessed by real-time polymerase chain reaction. Lightly pigmented human skin (L*>65) was exposed up to four times (one exposure/day) to UVA1 irradiation at a low-dose (20 J/cm2), mimicking UVA levels from strong sun exposure lasting approximately two hours. A single exposure to low-dose UVA1 irradiation darkened skin slightly, and did not alter MMP-1 or type I procollagen gene expression. With repeated low-dose UVA1 irradiation, skin darkened incrementally with each exposure. Despite this darkening, two or more exposures to low-dose UVA1 irradiation significantly induced MMP-1 gene expression, which increased progressively with successive exposures. Repeated UVA1 exposures did not suppress type I procollagen expression. A limited number of low-dose UVA1 exposures, as commonly experienced in daily life, potentially promotes photoaging by affecting breakdown, rather than synthesis, of collagen. Progressive skin darkening in response to repeated low-dose UVA1 exposures in lightly pigmented individuals does not prevent UVA1-induced collagenolytic changes. Therefore, for optimal protection against skin damage, sunscreen formulations should filter all UV wavelengths, including UVA1 irradiation.
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影响因子：
15.9
作者：
Fisher, GJ;Datta, S;Voorhees, JJ
通讯作者：
Voorhees, JJ
影响因子：
6.5
作者：
WESTERHOF, W;ESTEVEZUSCANGA, O;CARIO, I
通讯作者：
CARIO, I
影响因子：
158.5
作者：
Fisher, GJ;Wang, ZQ;Voorhees, JJ
通讯作者：
Voorhees, JJ
影响因子：
--
作者：
Fisher, Gary J.;Varani, James;Voorhees, John J.
通讯作者：
Voorhees, John J.
影响因子：
7.3
作者：
Beasley, Donathan G.;Meyer, Thomas A.
通讯作者：
Meyer, Thomas A.