Hepatic injury-specific conversion of mouse plasma hyaluronan binding protein to the active hetero-dimer form
Hepatic injury-specific conversion of mouse plasma hyaluronan binding protein to the active hetero-dimer form
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DOI：
10.1248/bpb.24.892
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发表时间：
2001-08-01
影响因子：
2
通讯作者：
Tomita, M
中科院分区：
文献类型：
--
作者：
Choi-Miura, NH;Otsuyama, K;Tomita, M
血浆透明质酸结合蛋白（PHBP）仅在小鼠肝脏和肾脏中产生。PHBP mRNA的诱导和前PHBP的活性异源二聚体形式的转换进行了研究后，四氯化碳，D-氨基半乳糖，氯化汞或turaldehyde管理和部分肝切除术后。结果表明，CCl_4和D-氨基半乳糖的给药，引起肝衰竭，肝部分切除，促进血浆中proPHBP向活性双链形式的转化。而HgCl_2损伤肾脏、损伤肾小管引起炎症反应，与PHBP的激活无关。肝脏中PHBP mRNA的表达在CCl4处理后3h和12h分别出现弱的诱导和抑制作用。HgCl 2和Turn4对PHBP mRNA表达量无明显影响。这些结果表明，肝损伤特异性激活血浆中的PHBP。PHBP可能是肝损伤后肝脏组织重建级联反应的早期因子，PHBP激活尿激酶，尿激酶激活基质金属蛋白酶（MMPs），MMPs降解细胞外基质用于肝再生。
Plasma hyaluronan binding protein (PHBP) is produced only in liver and kidney in mouse. The induction of PHBP mRNA and the conversion of pro PHBP to the active hetero-dimer form were studied after CCl4, D-galactosamine, HgCl2 or turpentine administration and after partial hepatectomy. The results indicated that the administrations of CCl4 and D-galactosamine, which caused hepatic failure, and the partial hepatectomy enhanced the conversion of pro PHBP to the active two-chain form in the plasma. On the other hand, HgCl2 which injured kidney and turpentine which led to inflammation were not involved in the activation of PHBP. The weak induction and suppression of PHBP mRNA were observed in the liver at 3 h and 12 h, respectively, after the CCl4 administration. However, HgCl2 and turpentine did not influence the amount of PHBP mRNA. These results suggested the hepatic injury-specific activation of PHBP in plasma. PHBP may act as an early factor in the cascade for the tissue remodeling in liver following hepatic injury, i.e., PHBP activates urokinase, urokinase activates matrix metalloproteinases (MMPs) and MMPs degrade extracellular matrix for liver regeneration.