Protective role of AQP3 in UVA-induced NHSFs apoptosis via Bcl2 up-regulation

Protective role of AQP3 in UVA-induced NHSFs apoptosis via Bcl2 up-regulation
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DOI:
10.1007/s00403-013-1324-y
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发表时间:
2013-07-01
影响因子:
3
通讯作者:
Li, Ji
Li, Ji
中科院分区:
医学3区
文献类型:
--
作者:
Xie, Hongfu;Liu, Fangfen;Li, Ji

文献摘要

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水通道蛋白-3(AQP 3)是一种水/甘油转运蛋白,可促进水、尿素和甘油的转运,可通过上调Bcl-2抑制砷诱导的细胞凋亡。然而,它是否有一个保护作用,在紫外线A(UVA)诱导的正常人皮肤成纤维细胞凋亡尚不清楚。在这项研究中,我们证明,温和的UVA治疗不能诱导氧化细胞应激和细胞凋亡的正常人皮肤成纤维细胞(NHSFs)过表达AQP 3。在严重的UVA照射后,当AQP 3水平降低时,氧化细胞应激和凋亡增加。我们还发现,沉默AQP 3使NHSFs对低剂量UVA敏感。过表达AQP 3对高剂量UVA诱导的氧化应激和细胞凋亡具有保护作用。此外,我们观察到Bcl-2可能参与UVA诱导的细胞凋亡。我们的研究结果表明,水/甘油转运蛋白AQP 3在抵抗UVA诱导的细胞凋亡中起作用。
Aquaporin-3 (AQP3), a water/glycerol-transporting protein that facilitates water, urea, and glycerol transport, can inhibit arsenite-induced apoptosis by up-regulating Bcl-2. However, whether it has a protective role in ultraviolet A (UVA)-induced apoptosis in normal human skin fibroblasts is not known. In this study, we demonstrate that mild UVA treatment fails to induce oxidative cell stress and apoptosis in normal human skin fibroblasts (NHSFs) overexpressing AQP3. After severe UVA irradiation, there was an increase in oxidative cell stress and apoptosis when AQP3 levels decreased. We also found that silencing AQP3 sensitized NHSFs to low-dose UVA. Overexpressing AQP3 was protective against high-dose UVA-induced oxidative stress and apoptosis. Besides, we observed that Bcl-2 may be involved in UVA-induced apoptosis. Our findings suggested that the water/glycerol-transporting protein AQP3 plays a role in resistance to UVA-induced apoptosis.