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硬皮病样胶原代谢改变发生于TSK(紧皮)小鼠。

Scleroderma-like alterations in collagen metabolism occurring in the TSK (tight skin) mouse.

作者信息

Jimenez S A, Millan A, Bashey R I

出版信息

Arthritis Rheum. 1984 Feb;27(2):180-5. doi: 10.1002/art.1780270209.

DOI:10.1002/art.1780270209
PMID:6696773
Abstract

Abnormalities in collagen metabolism similar to those occurring in the skin of patients with scleroderma have been demonstrated in the TSK (tight skin) mouse, a dominant mutant of the inbred B10.D2(58N)/SN mouse strain. These abnormalities, which consist of increased collagen content, accelerated biosynthesis, and increased extractibility of the newly synthesized molecules, suggest that the TSK mouse may be an excellent animal model for the study of the connective tissue alterations characteristic of scleroderma.

摘要

在近交系B10.D2(58N)/SN小鼠品系的显性突变体TSK(紧皮)小鼠中,已证实其胶原代谢异常与硬皮病患者皮肤中出现的异常相似。这些异常包括胶原含量增加、生物合成加速以及新合成分子的可提取性增加,这表明TSK小鼠可能是研究硬皮病特征性结缔组织改变的优秀动物模型。

相似文献

1
Scleroderma-like alterations in collagen metabolism occurring in the TSK (tight skin) mouse.硬皮病样胶原代谢改变发生于TSK(紧皮)小鼠。
Arthritis Rheum. 1984 Feb;27(2):180-5. doi: 10.1002/art.1780270209.
2
Increased collagen biosynthesis and increased expression of type I and type III procollagen genes in tight skin (TSK) mouse fibroblasts.紧致皮肤(TSK)小鼠成纤维细胞中胶原蛋白生物合成增加以及I型和III型前胶原基因表达增加。
J Biol Chem. 1986 Jan 15;261(2):657-62.
3
Immunological characterization of (tight skin/NZB)F1 hybrid mice with connective tissue and autoimmune features resembling human systemic sclerosis.
J Autoimmun. 1993 Jun;6(3):337-51. doi: 10.1006/jaut.1993.1029.
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Collagenous abnormalities in the heart of the tight-skin mouse.
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Anti-IL-4 treatment prevents dermal collagen deposition in the tight-skin mouse model of scleroderma.抗白细胞介素-4治疗可预防硬皮病紧皮小鼠模型中的真皮胶原沉积。
Eur J Immunol. 1998 Sep;28(9):2619-29. doi: 10.1002/(SICI)1521-4141(199809)28:09<2619::AID-IMMU2619>3.0.CO;2-M.
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Increased dermal elastic fibers in the tight skin mouse.紧致皮肤小鼠的真皮弹性纤维增加。
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The tight-skin mouse: physical and biochemical properties of the skin.
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Mast cell accumulation and cytokine expression in the tight skin mouse model of scleroderma.硬皮病紧密皮肤小鼠模型中的肥大细胞聚集和细胞因子表达。
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Mutant fibrillin 1 from tight skin mice increases extracellular matrix incorporation of microfibril-associated glycoprotein 2 and type I collagen.来自紧皮小鼠的突变原纤蛋白1增加了微原纤维相关糖蛋白2和I型胶原在细胞外基质中的掺入。
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Correlation between the concentration of serum anti-topoisomerase I autoantibodies and histological and biochemical alterations in the skin of tight skin mice.血清抗拓扑异构酶I自身抗体浓度与紧皮小鼠皮肤组织学及生化改变之间的相关性
Cell Immunol. 1996 Jan 10;167(1):135-40. doi: 10.1006/cimm.1996.0017.

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Curr Rheumatol Rep. 2016 Jan;18(1):4. doi: 10.1007/s11926-015-0553-9.
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Collagen content in skin and internal organs of the tight skin mouse: an animal model of scleroderma.紧皮小鼠皮肤和内脏器官中的胶原蛋白含量:硬皮病动物模型
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In perspective: murine models of scleroderma.透视:硬皮病的小鼠模型
Curr Rheumatol Rep. 2008 Jul;10(3):173-82. doi: 10.1007/s11926-008-0030-9.
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Fibrosis in systemic sclerosis.系统性硬化症中的纤维化
Rheum Dis Clin North Am. 2008 Feb;34(1):115-43; vii. doi: 10.1016/j.rdc.2007.11.002.
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New insights into the assembly of extracellular microfibrils from the analysis of the fibrillin 1 mutation in the tight skin mouse.通过对紧皮小鼠中纤连蛋白1突变的分析,对细胞外微原纤维组装的新见解。
J Cell Biol. 2000 Aug 7;150(3):667-80. doi: 10.1083/jcb.150.3.667.
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The Tight skin mouse: demonstration of mutant fibrillin-1 production and assembly into abnormal microfibrils.紧皮小鼠:突变型原纤蛋白-1的产生及组装成异常微原纤维的证明。
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Endothelial cell apoptosis is a primary pathogenetic event underlying skin lesions in avian and human scleroderma.内皮细胞凋亡是禽类和人类硬皮病皮肤病变潜在的主要致病事件。
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