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CD156 Transgenic Mice. different responses between inflammatory types.

机译:CD156转基因小鼠。炎症类型之间的反应不同。

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CD156 (ADAM8) is part of the ADAM family of proteins with the catalytic site consensus sequence of metalloprotease and disintegrins. To examine the role of CD156 in vivo, we generated mutant CD156 (eCD156) transgenic mice expressing the ectodomain of CD156 under the control of the alpha1-antitrypsin (AT) promoter. One of the transgenic mice designated ATMS2-TG18 expressed a 1.84 kb mRNA which was predicted to be a truncated CD156. The expression of the transgenic CD156 mRNA in ATMS2-TG18 mice was abundant in the liver and slight in kidney. Turpentine oil (TO) and lipopolysaccharide (LPS) markedly upregulated the expression. Soluble CD156 (sCD156) was produced constitutively, and increased after the treatment with TO. Casein-induced peritoneal leukocyte infiltration was significantly less extensive in ATMS2-TG18 than non-transgenic mice. The expression of L-selectin in neutrophils (PMN) from peripheral blood leukocytes (PBL) was more strongly downregulated in ATMS2-TG18 than non-transgenic mice, suggesting that L-selectin in PMN from ATMS2-TG18 mice was shed by sCD156. In contrast, oxazolone (Ox)-induced contact hypersensitivity reactions (CHR) were more marked in ATMS2-TG18 than non-transgenic mice. The expression of E-selectin mRNA was detected in inflammatory skin sites from ATMS2-TG18, but not non-transgenic mice, suggesting that sCD156 may activate the endothelial cells and lead to the upregulation of E-selectin. These results suggest that CD156 regulates leukocyte infiltration directly or indirectly.
机译:CD156(ADAM8)是ADAM蛋白质家族的一部分,具有金属蛋白酶和双整合蛋白的催化位点共有序列。为了检查CD156在体内的作用,我们生成了在α1-抗胰蛋白酶(AT)启动子的控制下表达CD156胞外域的突变CD156(eCD156)转基因小鼠。一只名为ATMS2-TG18的转基因小鼠表达了1.84 kb的mRNA,预计该基因是截短的CD156。 ATMS2-TG18小鼠中转基因CD156 mRNA的表达在肝脏中丰富,而在肾脏中则轻度表达。松节油(TO)和脂多糖(LPS)明显上调表达。可溶性CD156(sCD156)组成性地产生,并在用TO处理后增加。与非转基因小鼠相比,酪蛋白诱导的腹膜白细胞浸润在ATMS2-TG18中的扩散范围明显较小。与非转基因小鼠相比,ATMS2-TG18中外周血白细胞(PBL)中性粒细胞(PMN)中L-选择素的表达更强烈下调,这表明sCD156可以去除ATMS2-TG18小鼠PMN中的L-选择素。相反,在ATMS2-TG18中,恶唑酮(Ox)诱导的接触超敏反应(CHR)比非转基因小鼠更明显。在来自ATMS2-TG18的炎性皮肤部位中检测到E-选择素mRNA的表达,但在非转基因小鼠中未检测到,这表明sCD156可能激活内皮细胞并导致E-选择素的上调。这些结果表明CD156直接或间接调节白细胞浸润。

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