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Title:
Plasminogen Deficiency Leads to Impaired Remodeling after a Toxic Injury to the Liver
Authors:
Bezerra, Jorge A.; Bugge, Thomas H.; Melin-Aldana, Hector; Sabla, Gregg; Kombrinck, Keith W.; Witte, David P.; Degen, Jay L.
Affiliation:
AA(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AB(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AC(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AD(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AE(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AF(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039), AG(Children's Hospital Research Foundation and Department of Pediatrics, University of Cincinnati, OH 45229-3039)
Publication:
Proceedings of the National Academy of Sciences of the United States of America, Volume 96, Issue 26, 1999, pp.15143-15148
Publication Date:
12/1999
Origin:
JSTOR; PNAS
DOI:
10.1073/pnas.96.26.15143
Bibliographic Code:
1999PNAS...9615143B

Abstract

Cellular proliferation and tissue remodeling are central to the regenerative response after a toxic injury to the liver. To explore the role of plasminogen in hepatic tissue remodeling and regeneration, we used carbon tetrachloride to induce an acute liver injury in plasminogen-deficient (Plgo) mice and nontransgenic littermates (Plg+). On day 2 after CCl4, livers of Plg+ and Plgo mice had a similar diseased pale/lacy appearance, followed by restoration of normal appearance in Plg+ livers by day 7. In contrast, Plgo livers remained diseased for as long as 2.5 months, with a diffuse pale/lacy appearance and persistent damage to centrilobular hepatocytes. The persistent centrilobular lesions were not a consequence of impaired proliferative response in Plgo mice. Notably, fibrin deposition was a prominent feature in diseased centrilobular areas in Plgo livers for at least 30 days after injury. Nonetheless, the genetically superimposed loss of the Aalpha fibrinogen chain (Plgo/Fibo mice) did not correct the abnormal phenotype. These data show that plasminogen deficiency impedes the clearance of necrotic tissue from a diseased hepatic microenvironment and the subsequent reconstitution of normal liver architecture in a fashion that is unrelated to circulating fibrinogen.
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