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金属硫蛋白基因敲除小鼠在体内对紫外线B损伤的耐受性降低。

Metallothionein-null mice exhibit reduced tolerance to ultraviolet B injury in vivo.

作者信息

Wang W-H, Li L-F, Zhang B-X, Lu X-Y

机构信息

Department of Dermatology, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing 100083, China.

出版信息

Clin Exp Dermatol. 2004 Jan;29(1):57-61. doi: 10.1111/j.1365-2230.2004.01424.x.

DOI:10.1111/j.1365-2230.2004.01424.x
PMID:14723724
Abstract

Events that induce expression of the metallothionein (MT) gene, such as injection of cadmium chloride, cold stress or topical application of 1,25-dihydroxyvitamin D3, can deplete the number of ultraviolet (UV) B-induced sunburn cells (SBC) in mouse skin in vivo. MT-null mouse skin explants exhibit reduced tolerance to UVB injury in vitro. However, the in vivo response of MT-null mice to UVB injury has not been investigated. In the present study, we investigated the role of the MT gene on UVB injury in vivo. MT-null mice that are deficient in MT-I and MT-II genes were studied and compared with homozygous wild-type mice. Mouse dorsal skin was irradiated with 0.05, 0.70 and 1.40 J/cm2 UVB. The thickness of the dorsal skin was measured with a spring micrometer before and 24 h after UVB irradiation. In addition, SBC were counted 24 h after UVB irradiation. No significant difference was found in the change of skin thickness between MT-null mice and control mice irradiated with low-dose UVB (0.05 J/cm2) (Student's t-test, t = 1.519, P = 0.167). At higher doses (0.70 and 1.40 J/cm2), the skin of MT-null mice became much thicker than that of control mice (Student's t-test, t = 6.576, P < 0.01 and t = 3.142, P = 0.007, respectively). More SBC were detected in MT-null mice skin irradiated with the highest dose of UVB (1.40 J/cm2) (Student's t-test, t = 4.258, P < 0.01). These results suggest that the MT gene in mice has a photoprotective role in vivo.

摘要

诱导金属硫蛋白(MT)基因表达的事件,如注射氯化镉、冷应激或局部应用1,25 - 二羟基维生素D3,可在体内减少小鼠皮肤中紫外线(UV)B诱导的晒伤细胞(SBC)数量。MT基因敲除小鼠的皮肤外植体在体外对UVB损伤的耐受性降低。然而,MT基因敲除小鼠对UVB损伤的体内反应尚未得到研究。在本研究中,我们调查了MT基因在体内UVB损伤中的作用。研究了缺乏MT - I和MT - II基因的MT基因敲除小鼠,并与纯合野生型小鼠进行比较。用0.05、0.70和1.40 J/cm2的UVB照射小鼠背部皮肤。在UVB照射前和照射后24小时用弹簧测微计测量背部皮肤厚度。此外,在UVB照射后24小时对SBC进行计数。在用低剂量UVB(0.05 J/cm2)照射的MT基因敲除小鼠和对照小鼠之间,未发现皮肤厚度变化有显著差异(学生t检验,t = 1.519,P = 0.167)。在较高剂量(0.70和1.40 J/cm2)下,MT基因敲除小鼠的皮肤比对照小鼠厚得多(学生t检验,分别为t = 6.576,P < 0.01和t = 3.142,P = 0.007)。在用最高剂量UVB(1.40 J/cm2)照射的MT基因敲除小鼠皮肤中检测到更多的SBC(学生t检验,t = 4.258,P < 0.01)。这些结果表明,小鼠中的MT基因在体内具有光保护作用。

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Metallothionein-null mice exhibit reduced tolerance to ultraviolet B injury in vivo.金属硫蛋白基因敲除小鼠在体内对紫外线B损伤的耐受性降低。
Clin Exp Dermatol. 2004 Jan;29(1):57-61. doi: 10.1111/j.1365-2230.2004.01424.x.
2
Photoprotective role of metallothionein in UV-injury - metallothionein-null mouse exhibits reduced tolerance against ultraviolet-B.
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Novel function of metallothionein in photoprotection: metallothionein-null mouse exhibits reduced tolerance against ultraviolet B injury in the skin.
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Possible role of 1,25-dihydroxyvitamin D3-induced metallothionein in photoprotection against UVB injury in mouse skin and cultured rat keratinocytes.1,25-二羟基维生素D3诱导的金属硫蛋白在小鼠皮肤和培养的大鼠角质形成细胞中对紫外线B损伤的光保护作用中的可能作用。
J Dermatol Sci. 1995 May;9(3):203-8. doi: 10.1016/0923-1811(94)00378-r.
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Protective effects of cadmium chloride against UVB injury in mouse skin and in cultured human cells: a possible role of cadmium-induced metallothionein.氯化镉对小鼠皮肤和培养的人细胞中紫外线B损伤的保护作用:镉诱导的金属硫蛋白的可能作用。
Photodermatol Photoimmunol Photomed. 1991 Jun;8(3):111-5.
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Lack of metallothionein-I and -II exacerbates the immunosuppressive effect of ultraviolet B radiation and cis-urocanic acid in mice.金属硫蛋白-I和-II的缺乏会加剧紫外线B辐射和顺式尿刊酸对小鼠的免疫抑制作用。
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Topical tocopherol acetate reduces post-UVB, sunburn-associated erythema, edema, and skin sensitivity in hairless mice.局部应用醋酸生育酚可减轻无毛小鼠紫外线B照射后晒伤相关的红斑、水肿和皮肤敏感性。
Arch Biochem Biophys. 1992 Aug 1;296(2):575-82. doi: 10.1016/0003-9861(92)90613-2.
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The effect of cold stress on UVB injury in mouse skin and cultured keratinocytes.冷应激对小鼠皮肤及培养的角质形成细胞中紫外线B损伤的影响。
Photochem Photobiol. 1996 Dec;64(6):984-7. doi: 10.1111/j.1751-1097.1996.tb01865.x.
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The study of ultraviolet B-induced apoptosis in cultured mouse keratinocytes and in mouse skin.紫外线B诱导培养的小鼠角质形成细胞及小鼠皮肤细胞凋亡的研究
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Metallothionein I and II gene knock-out mice exhibit reduced tolerance to 24-h sodium lauryl sulphate patch testing.金属硫蛋白I和II基因敲除小鼠对24小时月桂醇硫酸酯钠斑贴试验的耐受性降低。
Clin Exp Dermatol. 2007 Jul;32(4):417-22. doi: 10.1111/j.1365-2230.2007.02399.x. Epub 2007 Mar 14.

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