Extracellular matrix alteration in chronic hepatitis.
Chia Hsing, F J Leu, Tang‐Yi Tsao, J Wang, Hong Tang
Abstract
Chia Hsing, F J Leu, Tang‐Yi Tsao, J Wang, Hong Tang
Abstract
We used immunofluorescence and immunohistochemical PAP methods on 22 paraffin-embedded liver tissue specimens for observation and analysis of the distribution of extracellular matrix (ECM) elements in chronic hepatitis and cirrhosis. Our study revealed that in CLH there was only mild increases of types III, V collagen and fibronectin in spotty necrosis areas. In CPH, types III, V collagen and fibronectin revealed mild to moderate increase in portal area and lobular sinusoid. In CAH, moderate to marked increases of types III, V collagen and fibronectin and mild increase of type IV collagen in portal area, sinusoid lining, piecemeal necrosis and fibroseptum were found. Types I, IV collagen in fibroseptum were also noted. Some periportal hepatocytes showed abundant intracellular fibronectin. In cirrhosis, cases expressed similar finding to CAH except much more type IV collagen deposition. In addition, the basement membrane components including type IV collagen and laminin were found in the "capillarization" of periportal sinusoids in fibrotic liver tissue. In areas of piecemeal necrosis, the hepatocytes, single or assembled in "rosettes", were underlined by linear deposits of laminin and type IV collagen. Our study revealed that, histologically, the ECMs distribution of CAH is similar to that of cirrhosis but could be clearly distinguished from CPH and CLH. The prominent changes of ECMs, especially the basement membrane components, in case of CAH and cirrhosis are consistent with the fact that ECM may play a central role in liver function impairment and fibrogenesis.
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We used immunofluorescence and immunohistochemical PAP methods on 22 paraffin-embedded liver tissue specimens for observation and analysis of the distribution of extracellular matrix (ECM) elements in chronic hepatitis and cirrhosis. Our study revealed that in CLH there was only mild increases of types III, V collagen and fibronectin in spotty necrosis areas. In CPH, types III, V collagen and fibronectin revealed mild to moderate increase in portal area and lobular sinusoid. In CAH, moderate to marked increases of types III, V collagen and fibronectin and mild increase of type IV collagen in portal area, sinusoid lining, piecemeal necrosis and fibroseptum were found. Types I, IV collagen in fibroseptum were also noted. Some periportal hepatocytes showed abundant intracellular fibronectin. In cirrhosis, cases expressed similar finding to CAH except much more type IV collagen deposition. In addition, the basement membrane components including type IV collagen and laminin were found in the "capillarization" of periportal sinusoids in fibrotic liver tissue. In areas of piecemeal necrosis, the hepatocytes, single or assembled in "rosettes", were underlined by linear deposits of laminin and type IV collagen. Our study revealed that, histologically, the ECMs distribution of CAH is similar to that of cirrhosis but could be clearly distinguished from CPH and CLH. The prominent changes of ECMs, especially the basement membrane components, in case of CAH and cirrhosis are consistent with the fact that ECM may play a central role in liver function impairment and fibrogenesis.
Key concepts: Fibronectin, Laminin, Basement membrane, Type IV collagen, Extracellular matrix, Cirrhosis, Pathology, Sinusoid