Hepatic Injury-Specific Conversion of Mouse Plasma Hyaluronan Binding Protein to the Active Hetero-Dimer Form

• Published in: Biological & pharmaceutical bulletin 2001, Vol.24(8), pp.892-896
• Main Authors: CHOI-MIURA, Nam-Ho, OTSUYAMA, Kayo, SANO, Yoshihiro, SAITO, Kiyomi, TAKAHASHI, Katsuhiko, TOMITA, Motowo
• Format: Article
• Language: English
• Subjects: activation; Animals; Biological and medical sciences; Biotransformation; Blotting, Northern; Blotting, Western; Carbon Tetrachloride Poisoning - metabolism; Carbon Tetrachloride Poisoning - pathology; Chemical and Drug Induced Liver Injury - metabolism; Chemical and Drug Induced Liver Injury - pathology; Chemical and industrial products toxicology. Toxic occupational diseases; DNA Probes; Gastroenterology. Liver. Pancreas. Abdomen; hepatic injury; Hyaluronan Receptors - biosynthesis; Hyaluronan Receptors - blood; Hyaluronan Receptors - genetics; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Medical sciences; Mercuric Chloride - toxicity; Mice; Other diseases. Semiology; PHBP; Recombinant Proteins - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - biosynthesis; serine protease; tissue remodeling; Toxicology; Various organic compounds
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.24.892

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.