Mechanism of acute depletion of plasma fibronectin following thermal injury in rats. Appearance of a gelatinlike ligand in plasma.
Mechanism of acute depletion of plasma fibronectin following thermal injury in rats. Appearance of a gelatinlike ligand in plasma.
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大鼠热损伤后血浆纤连蛋白急性耗竭的机制。
DOI：
10.1172/jci111191
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Blumenstock,FA
中科院分区：
文献类型：
--
作者：
Deno,DC;McCafferty,MH;Saba,TM;Blumenstock,FA
麻醉大鼠在亚致死烧伤后 15 分钟内血浆纤连蛋白耗尽，8 小时部分恢复，24 小时完全恢复。放射性标记的 75Se-血浆纤连蛋白在烧伤前静脉注射，很快被隔离在烧伤皮肤和肝脏中。通过免疫测定法检测到的烧伤后 2 小时的纤连蛋白水平与 75Se 血浆纤连蛋白的水平表明，血浆中的纤连蛋白比通过电免疫测定法检测到的要多。对烧伤后早期血浆中纤连蛋白的交叉免疫电泳分析表明纤连蛋白抗原的电泳迁移率降低。在正常血浆中添加肝素或纤维蛋白（两者都对纤连蛋白具有亲和力）无法重现这种改变的纤连蛋白电泳模式。相反，在正常血浆中添加明胶或天然胶原蛋白会重现烧伤血浆中纤连蛋白的异常电泳模式。当将烧伤皮肤的提取物（而非正常皮肤的提取物）添加到正常血浆中时，会引发类似的纤连蛋白电泳模式改变。通过凝胶过滤，烧伤血浆中纤连蛋白的表观分子量比正常血浆中观察到的高约 40%。这些数据表明烧伤皮肤中的明胶样配体释放到血液中，与血浆纤连蛋白复合。因此，烧伤后纤连蛋白急性缺乏似乎是由以下因素介导的：(a)纤连蛋白在烧伤部位的积累； (b) 通过肝脏将其从循环中去除； (c) 它以免疫测定法不易检测到的形式存在于血浆中。
Plasma fibronectin was depleted within 15 min following sublethal burn, followed by partial recovery at 8 h and complete restoration by 24 h in anesthetized rats. Radiolabeled 75Se-plasma fibronectin, injected intravenously before burn, was rapidly sequestered in burn skin as well as the liver. Fibronectin levels at 2 h postburn as detected by immunoassay vs. 75Se-plasma fibronectin indicated that more fibronectin was in the plasma than detected by electroimmunoassay. Crossed immunoelectrophoretic analysis of fibronectin in early postburn plasma demonstrated a reduced electrophoretic mobility of the fibronectin antigen. Addition of heparin or fibrin, both of which have affinity for fibronectin, to normal plasma was unable to reproduce this altered fibronectin electrophoretic pattern. In contrast, addition of gelatin or native collagen to normal plasma reproduced the abnormal electrophoretic pattern of fibronectin seen in burn plasma. Extracts of burned skin, but not extracts of normal skin, when added to normal plasma, elicited a similar altered electrophoretic pattern for fibronectin. By gel filtration, fibronectin in burn plasma had an apparent molecular weight approximately 40% greater than that observed in normal plasma. These data suggest the release into the blood of a gelatinlike ligand from burned skin, which complexes with plasma fibronectin. Thus, fibronectin deficiency acutely postburn appears mediated by (a) its accumulation at the site of burn injury; (b) its removal from the circulation by the liver; and (c) its presence in the plasma in a form that is less detectable by immunoassay.Images