Infrared‐A (IRA), which can penetrate deeply into the human skin, is a major component of solar radiation and is recognized to promote photoaging of human dermis. To our knowledge, however, the cellular and molecular consequences of human epidermis exposure to IRA have not been clarified. Thus, we investigated whether IRA inhibits the proliferation of normal human epidermal keratinocytes (NHEKs). IRA irradiation ed in cell cycle arrest at G1 and a dose‐dependent reduction in the proliferation of NHEKs. We found that mechanistic target of rapamycin complex 1 (mTORC1) was initially inactivated during IRA irradiation due to the formation of stress granules (SGs), and this inactivation was maintained for at least 6 h after irradiation due to Akt dephosphorylation. Furthermore, repeated exposure of human skin equivalents to IRA led to marked thinning of the epidermal cell layer. In conclusion, IRA irradiation inhibits mTORC1 activity possibly through two molecular mechanisms involving SG formation in the early‐phase and subsequent Akt dephosphorylation. This sequential mechanism seems to cause G1 cell cycle arrest and a reduction in cell proliferation, supporting the hypothesis that the decreased proliferation of basal keratinocytes that occurs during skin aging might be partly attributable to IRA radiation.

中文翻译：

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红外-A 辐射诱导的人角质形成细胞增殖抑制和潜在机制

红外线 (IRA) 可以深入人体皮肤，是太阳辐射的主要成分，被认为可以促进人体真皮的光老化。然而，据我们所知，人类表皮暴露于 IRA 的细胞和分子后果尚未阐明。因此，我们研究了 IRA 是否抑制正常人表皮角质形成细胞 (NHEK) 的增殖。IRA 照射导致细胞周期停滞在 G1 和剂量依赖性减少 NHEK 的增殖。我们发现雷帕霉素复合物 1 (mTORC1) 的机制靶标在 IRA 照射期间由于应力颗粒 (SGs) 的形成而最初失活，并且由于 Akt 去磷酸化，这种失活在照射后维持至少 6 小时。此外，人体皮肤等价物反复暴露于 IRA 导致表皮细胞层显着变薄。总之，IRA 照射可能通过两种分子机制抑制 mTORC1 活性，包括早期 SG 形成和随后的 Akt 去磷酸化。这种顺序机制似乎导致 G1 细胞周期停滞和细胞增殖减少，支持了皮肤老化过程中基底角质形成细胞增殖减少可能部分归因于 IRA 辐射的假设。