Background:

MiR-664 has been demonstrated to play an important role in dermal diseases. However, the functions of miR-664 in ultraviolet B (UVB) radiation-induced keratinocytes damage remain to be elucidated.

Objective:

The present study aimed to investigate the molecular mechanisms under the UVB-induced keratinocytes damage and provide translational insights for future therapeutics and UVB protection.

Methods:

HaCaT cells were transfected with miR-664, either alone or combined with UVB irradiation. Levels of messenger RNA and protein were tested by quantitative real-time polymerase chain reaction and Western blot analyses. Cell proliferation, percentage of apoptotic cells, and expression levels of apoptosis-related factors were measured by Cell Counting Kit-8 assay, flow cytometry assay, and Western blot analysis, respectively.

Results:

We found that a significant increase in miR-664 was observed in UVB-induced HaCaT cells. Overexpressed miR-664 promoted cell vitalities and suppressed apoptosis of UVB-induced HaCaT cells. Additionally, the loss/gain of armadillo-repeat-containing protein 8 (ARMC8) rescued/blocked the effects of miR-664 on the proliferation of UVB-induced HaCaT cells.

Conclusions:

Our data demonstrate that miR-664 functions as a protective regulator in UVB-induced HaCaT cells via regulating ARMC8.

中文翻译：

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MiR-664 通过下调 ARMC8 防止 UVB 辐射诱导的 HaCaT 细胞损伤。

背景：

MiR-664 已被证明在皮肤疾病中发挥重要作用。然而，miR-664 在紫外线 B (UVB) 辐射诱导的角质形成细胞损伤中的功能仍有待阐明。

客观的：

本研究旨在研究 UVB 诱导的角质形成细胞损伤的分子机制，并为未来的治疗和 UVB 保护提供转化见解。

方法：

HaCaT 细胞用 miR-664 转染，单独或与 UVB 照射组合。通过定量实时聚合酶链反应和蛋白质印迹分析测试信使 RNA 和蛋白质的水平。细胞增殖、凋亡细胞百分比和凋亡相关因子的表达水平分别通过 Cell Counting Kit-8 测定、流式细胞术测定和蛋白质印迹分析进行测量。

结果：

我们发现在 UVB 诱导的 HaCaT 细胞中观察到 miR-664 的显着增加。过表达的 miR-664 可促进细胞活力并抑制 UVB 诱导的 HaCaT 细胞的凋亡。此外，含犰狳重复蛋白 8 (ARMC8) 的丢失/获得挽救/阻止了 miR-664 对 UVB 诱导的 HaCaT 细胞增殖的影响。

结论：

我们的数据表明，miR-664 通过调节 ARMC8 在 UVB 诱导的 HaCaT 细胞中起到保护性调节剂的作用。