Relationship between serum and hepatic 7S fragments of type IV collagen in chronic liver disease

✍ Scribed by T Suou; S Yamada; K Hosho; N Yoshikawa; H Kawasaki

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 200 KB
• Volume: 23
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.510230533

✦ Synopsis

We evaluated the mechanism of increased serum con-gens can cause increased levels of serum collagen-recentrations of the 7S fragment of the N-terminal domain lated antigens such as the 7S fragment of the Nof type IV collagen (7S collagen) in chronic liver disease. terminal domain of type IV collagen (7S collagen). 4 We measured the concentrations of hepatic-free and de-Type IV collagen is a main collagenous component of posited 7S collagens after extraction with Tris-HCl the basement membrane. It is synthetized primarily in buffer and bacterial collagenase, then compared them the fat-storing cells [5][6][7] and degraded in the migrating with the serum levels in 8 normal controls and 48 paendothelial cells. 8 7S collagen is the major cross-linking tients with chronic liver disease. The hepatic 7S collagen domain of type IV collagen and is not cleaved off during levels extracted with Tris-HCl buffer and collagenase the assembly of type IV collagen. Each 7S collagen molaccounted for 7% and 93%, respectively, of the total 7S ecule connects four type IV collagens by their N-termicollagen levels in normal controls. Both hepatic 7S collagen levels as well as serum levels increased in accor-nal regions. 9 Serum 7S collagen is thus thought to be dance with the progress of liver disease. Serum levels of derived from either the degradation of extant basement 7S collagen showed a closer correlation with the hepatic membrane, from newly formed type IV collagen that is 7S collagen levels extracted with Tris-HCl buffer (r not being deposited in the tissue, or both. 4 Å .822), compared with those extracted with collagenase