Characterization of the inbred CE/J mouse strain as amyloid resistant.

Characterization of the inbred CE/J mouse strain as amyloid resistant.
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DOI:
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发表时间:
1993-11
期刊:
The American journal of pathology
影响因子:
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通讯作者:
J. D. Sipe;Isabel Carreras;W. Gonnerman;Edgar S. Cathcart;Maria C. de;Beer;Frederick C. de
J. D. Sipe;Isabel Carreras;W. Gonnerman;Edgar S. Cathcart;Maria C. de;Beer;Frederick C. de
中科院分区:
其他
文献类型:
--
作者:
J. D. Sipe;Isabel Carreras;W. Gonnerman;Edgar S. Cathcart;Maria C. de;Beer;Frederick C. de

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相似文献

相对于五种常用的近交系A/J、CBA/J、C57 BL/6 J、C3 H/HeN和SJL/J,近交系CE/J小鼠已被鉴定为对偶氮酪蛋白诱导的淀粉样变性具有极强的抗性。CE/J小鼠中增强的淀粉样蛋白抗性似乎来源于CE/J小鼠中SAA基因家族的新结构,通过对SAA基因结构的Southern印迹杂交分析和对6个近交系中的急性期SAA蛋白的等电聚焦分析来确定。在CE/J小鼠中,存在pI 6.15的单一的新型SAA同种型,而在其他品系中,淀粉样蛋白生成性SAA 2同种型(pI 6.3)与SAA 1(pI 6.45)共显性表达。另外两个近交系,秘鲁和IS/CAM,与CE/J小鼠共享共同的SAA特异性HindIII DNA片段。野生小家鼠不同于所有的近交系研究,无论是在SAA基因结构和SAA亚型生产的模式;两种亚型,一个PI 6.15和其他PI 6.3(对应于SAA 2),共显性表达。CE/J小鼠对脂多糖、酪蛋白、硝酸银、白细胞介素-1或肿瘤坏死因子的反应仅产生pI 6.15亚型,而非SAA 1和2;肿瘤坏死因子对pI 6.15亚型的刺激作用弱于白细胞介素-1,因为它对其他近交系中SAA 1和2的产生也是如此。本研究提供了一个新的证据支持的作用,前体结构作为一个决定因素,在小鼠淀粉样蛋白A淀粉样变性,并提供了一个有价值的模型,淀粉样蛋白的研究。
Inbred CE/J mice have been identified as extremely resistant to azocasein-induced amyloidosis relative to five commonly used inbred strains, A/J, CBA/J, C57BL/6J, C3H/HeN, and SJL/J. The enhanced amyloid resistance in CE/J mice seems to derive from the novel structure of the SAA gene family in CE/J mice, as determined by Southern blot hybridization analysis of SAA gene structure and isoelectric focusing analysis of acute phase SAA proteins in the six inbred strains. In CE/J mice, a single, novel SAA isoform of pI 6.15 is present, whereas in the other strains the amyloidogenic SAA2 isoform (pI 6.3) is codominantly expressed with SAA1 (pI 6.45). Two other inbred strains, PERU and IS/CAM, share common SAA specific HindIII DNA fragments with CE/J mice. Wild-derived Mus musculus mice differ from all of the inbred strains studied, both in SAA gene structure and in the pattern of SAA isoform production; two isoforms, one pI 6.15 and the other pI 6.3 (corresponding to SAA2), were codominantly expressed. Only the pI 6.15 isoform, not SAA1 and 2, was produced by CE/J mice in response to lipopolysaccharide, casein, silver nitrate, interleukin-1, or tumor necrosis factor; tumor necrosis factor was a weaker stimulus than interleukin-1 for the pI 6.15 isoform as it is for SAA1 and 2 production in the other inbred strains. This study provides a new line of evidence supporting the role of precursor structure as a determining factor in murine amyloid A amyloidosis and provides a valuable model for studies of amyloidogenesis.