TGF-β1 mediates 70-kDa heat shock protein induction due to ultraviolet irradiation in human skin fibroblasts

TGF-β1 mediates 70-kDa heat shock protein induction due to ultraviolet irradiation in human skin fibroblasts
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DOI:
10.1007/s004240050905
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发表时间:
1999-08-01
影响因子:
4.5
通讯作者:
Yamashita, S
Yamashita, S
中科院分区:
医学3区
文献类型:
--
作者:
Cao, Y;Ohwatari, N;Yamashita, S

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紫外线B (UVB)改变人皮肤成纤维细胞热休克蛋白70 (HSP70)的表达。然而,信号转导途径的性质仍有待确定。转化生长因子- β (tgf - β)具有多种生物学功能,包括细胞生长控制、炎症调节和免疫调节。在这项研究中,我们研究了tgf - β是否与UVB照射诱导的HSP70表达过程有关。采用逆转录聚合酶链反应(RT-PCR)和Western blot方法检测人皮肤成纤维细胞tgf - β 1 mRNA的组成表达和HSP70的表达。结果表明:(1)UVB照射刺激HSP70表达呈剂量和时间依赖性;(2)UVB照射后检测到tgf - β 1 mRNA的组成性表达,在10 mJ cm(-2) UVB照射后4 h达到峰值;(3)未UVB照射的tgf - β 1诱导HSP70表达;(4)抗tgf - β II型受体抗体预孵育细胞抑制UVB照射诱导HSP70表达。我们的研究结果表明,UVB诱导的HSP70表达涉及tgf - β产生的自分泌信号传导。
Ultraviolet B (UVB) alters the expression of heat shock protein 70 (HSP70) in cultured fibroblast cells derived from human skin. However, the nature of the signal transduction pathway remains to be determined. Transforming growth factor-beta (TGF-beta) has a large variety of biological functions, including cell growth control, modulation of inflammation and immunoregulation. In this study, we examined whether TGF-beta is associated with the process of HSP70 expression induced by UVB irradiation. The constitutive expression of TGF-beta 1 mRNA and HSP70 expression in human skin fibroblast cells were detected using reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. The results indicate that: (1) UVB irradiation stimulates HSP70 expression in a dose- and time-dependent manner, (2) constitutive expression of TGF-beta 1 mRNA is detected after UVB irradiation, the level of which peaks at 4 h after 10 mJ cm(-2) of UVB irradiation, (3) HSP70 expression is induced by TGF-beta 1 without UVB irradiation, and (4) HSP70 expression induction with UVB irradiation is inhibited by preincubation of the cells with the anti-TGF-beta type II receptor antibody. Our results suggest that HSP70 expression induced by UVB involves the autocrine signalling of TGF-beta production.