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首页> 外文期刊>Journal of Cellular Physiology >Protease nexin I expression is up-regulated in human skeletal muscle by injury-related factors.
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Protease nexin I expression is up-regulated in human skeletal muscle by injury-related factors.

机译：蛋白酶nexin我表达是上调人类骨骼肌与伤害有关的因素。

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摘要

Protease nexin I is a 43-50 kDa glycoprotein capable of inhibiting a number of serine proteases. In cultured differentiated human skeletal muscle (myotubes), we previously found that protease nexin I was localized in patches at their surface where it was active and able to inhibit thrombin. To understand the role of skeletal muscle protease nexin I after injury or in inflammatory conditions where thrombin might be extravasated by blood vessels, we examined the role of inflammatory factors on protease nexin I synthesis and secretion by myotubes in culture. By enzyme-linked immunosorbent assay (ELISA) and Western blotting, we found that this serine protease inhibitor is secreted by cultured human myotubes. Protease nexin I secretion is stimulated by tumor necrosis factor-alpha, transforming growth factor-beta and interleukin-1. Complex formation experiments with labeled thrombin reveal active protease nexin I bound to the surface of the treated cells. Secreted protease nexin I-thrombin complex was enhanced in the presence of transforming growth factor-beta and tumor necrosis factor-alpha. Protease nexin I mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot analysis. Whatever the conditions, no significantly different levels were observed, indicating that the changes in cell and media protease nexin I concentration are elicited at the translational/posttranslational levels. Immunocytochemical studies on human skeletal muscle biopsies of patients suffering from inflammatory myopathies showed an overexpression of protease nexin I together with the above inflammatory factors. These findings suggest that skeletal muscle protease nexin I might play a role after injury or inflammatory pathologies.
机译：蛋白酶nexin我是43-50 kDa糖蛋白能够抑制丝氨酸蛋白酶。我们之前发现,骨骼肌(肌管),蛋白酶nexin我本地化补丁其表面活性,能够抑制凝血酶。骨骼肌蛋白酶nexin我受伤或后在炎症条件下凝血酶可能在哪里由血管,,我们检查了炎症因子在蛋白酶nexin我的角色合成和分泌的肌管文化。通过酶联免疫吸附试验(ELISA)和免疫印迹,我们发现这个丝氨酸蛋白酶抑制剂是由人工培养的分泌肌管。刺激肿瘤坏死因子-α,转化生长因子和interleukin-1。凝血酶标记揭示活性蛋白酶nexin我绑定到表面的细胞治疗。分泌蛋白酶nexin I-thrombin复杂增强的转变增长因子和肿瘤坏死因子-α。蛋白酶nexin我信使rna被逆转聚合酶链反应(rt - pcr),和北部污点分析。条件,没有明显不同观察,表明变化的细胞和媒体蛋白酶nexin我浓度在平移/转译后的了的水平。骨骼肌活检的患者从炎性肌病显示超表达蛋白酶nexin我一起上述炎症因素。表明骨骼肌蛋白酶nexin我可能损伤或炎症后发挥作用pathologies。

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