Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Hepatic injury-specific conversion of mouse plasma hyaluronan binding protein to the active hetero-dimer form. 1151 Apr 80

We have tested the ability of bone marrow (BM) cells (BMCs) to form hepatocytes in liver injury models. We used three models: (i) carbon tetrachloride (CCl4) treatment, (ii) albumin-urokinase transgenic mouse [TgN(Alb1Plau)], and (iii) hepatitis B transgenic mouse [TgN(Alb1HBV)]. As a nonselective liver injury model, irradiated C57BL/6 (B6) mice were transplanted with BMCs from GFP transgenic mouse [TgN(ActbEGFP)] or beta-galactosidase transgenic mouse [TgN(MtnLacZ)] followed by the administration of CCl4. Irradiated TgN(Alb1HBV) and TgN(Alb1Plau) were also transplanted with BMCs from TgN(ActbEGFP) or TgN(MtnLacZ). Approximately 1.5 x 106 hepatocytes per liver were analyzed for GFP-positive cells, and the whole livers were inspected for beta-galactosidase expression. No GFP-positive hepatocytes and no gross blue staining of the livers with 5-bromo-4-chloro-3-indolyl beta-d-galactoside in any of the 18 recipient mice analyzed were detected. The livers from female animals with gender-mismatched BM transplantation were also tested with Y chromosome fluorescent in situ hybridization analysis to detect donor-derived cells. A total of five isolated hepatocytes were positive for Y chromosome in 4.1 x 105 hepatocytes analyzed. Our results demonstrate that there is little or no contribution of BMCs to the replacement of injured livers in these models. We conclude that BM-derived cells cannot generally lead to a cure of liver damage.
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PMID:Little evidence of bone marrow-derived hepatocytes in the replacement of injured liver. 1523 8