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Kupffer cell prostaglandin‐E 2 production is amplified during hepatic regeneration
Author(s) -
Callery Mark P.,
Mangino Martin J.,
Flye M. Wayne
Publication year - 1991
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840140225
Subject(s) - regeneration (biology) , prostaglandin e2 , microbiology and biotechnology , kupffer cell , prostaglandin , chemistry , medicine , biology
Prostaglandin‐E 2 increases in liver tissue after partial hepatectomy and stimulates DNA synthesis in primary cultures of hepatocytes. This study evaluated the capacity of Kupffer cells isolated at various intervals after partial hepatectomy to produce prostaglandin E 2 in response to bacterial endotoxin. This stimulator of Kupffer cells is a normal endogenous component of portal venous blood. After partial hepatectomy (6 to 48 hr), when hepatic regeneration rates were greatest, regenerating liver Kupffer cells demonstrated a significantly greater capacity to produce prostaglandin E 2 in response to bacterial endotoxin than did equal numbers of Kupffer cells from timematched, sham‐operated control animals. However, by 12 days after partial hepatectomy, when liver mass had been more than 83% restored, regenerating liver Kupffer cell prostaglandin E 2 production had decreased to levels produced by sham KC. We postulate that high levels of Kupffer cell—derived prostaglandin E 2 provide a critical paracrine signal fundamental to the initiation and control of growth by neighboring hepatocytes during liver regeneration. (HEPATOLOGY 1991;14:368–372.)