Bone marrow–derived cells express matrix metalloproteinases and contribute to regression of liver fibrosis in mice

Reiichi Higashiyama, Yutaka Inagaki, Yun Yu Hong, Miwa Kushida, Sachie Nakao, Maki Niioka, Tetsu Watanabe, Hideyuki Okano, Yumi Matsuzaki, Goshi Shiota, Isao Okazaki – 22 December 2006 – Liver fibrosis is usually progressive, but it can occasionally be reversible if the causative agents are adequately removed or if patients are treated effectively. However, molecular mechanisms responsible for this reversibility of liver fibrosis have been poorly understood.

Linkage between a new splicing site mutation in the MDR3 alias ABCB4 gene and intrahepatic cholestasis of pregnancy

Gudrun Schneider, Teresa C. Paus, Gerd A. Kullak‐Ublick, Peter J. Meier, Thomas F. Wienker, Thomas Lang, Patricia van de Vondel, Tilman Sauerbruch, Christoph Reichel – 22 December 2006 – Intrahepatic cholestasis of pregnancy (ICP) is defined as pruritus and elevated bile acid serum concentrations in late pregnancy. Splicing mutations have been described in the multidrug resistance p‐glycoprotein 3 (MDR3, ABCB4) gene in up to 20% of ICP women. Pedigrees studied were not large enough for linkage analysis.

Hepatitis B virus promotes hepatocarcinogenesis in transgenic mice

Yanyan Zheng, Wen‐ling Chen, Stan G. Louie, T. S. Benedict Yen, Jing‐hsiung James Ou – 22 December 2006 – HBV is a major risk factor for hepatocellular carcinoma (HCC). However, whether HBV can directly cause HCC or only indirectly via the induction of chronic liver inflammation has been controversial. By using transgenic mice carrying the entire HBV genome as a model, we now demonstrate that HBV by itself is an inefficient carcinogen. However, it can efficiently promote hepatocarcinogenesis initiated by the carcinogen diethylnitrosamine (DEN).

Anti‐gp210 and anti‐centromere antibodies are different risk factors for the progression of primary biliary cirrhosis

Minoru Nakamura, Hisayoshi Kondo, Tsuyoshi Mori, Atsumasa Komori, Mutsumi Matsuyama, Masahiro Ito, Yasushi Takii, Makiko Koyabu, Terufumi Yokoyama, Kiyoshi Migita, Manabu Daikoku, Seigo Abiru, Hiroshi Yatsuhashi, Eiichi Takezaki, Naohiko Masaki, Kazuhiro Sugi, Koichi Honda, Hiroshi Adachi, Hidehiro Nishi, Yukio Watanabe, Yoko Nakamura, Masaaki Shimada, Tatsuji Komatsu, Akira Saito, Takeo Saoshiro, Hideharu Harada, Takeshi Sodeyama, Shigeki Hayashi, Akihide Masumoto, Takehiro Sando, Tetsuo Yamamoto, Hironori Sakai, Masakazu Kobayashi, Toyokichi Muro, Michiaki Koga, Zakera Shums, Gary L.

Immune role of hepatic TLR‐4 revealed by orthotopic mouse liver transplantation

Beena John, Ingo Klein, I. Nicholas Crispe – 22 December 2006 – Activated CD8+ T cells migrate to the liver at the end of an immune response and go through apoptosis there, but this mechanism is impaired in mice lacking Toll‐like receptor‐4. This allowed us to test the importance of liver trapping in an ongoing immune response. In the absence of Toll‐like receptor‐4, reduced liver accumulation was associated with an increase in the circulating CD8+ T cell pool, more long‐lived memory T cells and increased CD8+ T cell memory responses.

Thyroid hormone preconditioning: Protection against ischemia‐reperfusion liver injury in the rat

Virginia Fernández, Iván Castillo, Gladys Tapia, Pamela Romanque, Sebastián Uribe‐Echevarría, Mario Uribe, Denise Cartier‐Ugarte, Gonzalo Santander, María T. Vial, Luis A. Videla – 22 December 2006 – Recently, we reported that oxidative stress due to 3,3′,5‐triiodothyronine (T3)‐induced calorigenesis up‐regulates the hepatic expression of mediators promoting cell protection.

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