Mcl‐1 and Bcl‐xL cooperatively maintain integrity of hepatocytes in developing and adult murine liver

Hayato Hikita, Tetsuo Takehara, Satoshi Shimizu, Takahiro Kodama, Wei Li, Takuya Miyagi, Atsushi Hosui, Hisashi Ishida, Kazuyoshi Ohkawa, Tatsuya Kanto, Naoki Hiramatsu, Xiao‐Ming Yin, Lothar Hennighausen, Tomohide Tatsumi, Norio Hayashi – 28 September 2009 – Anti‐apoptotic members of the Bcl‐2 family, including Bcl‐2, Bcl‐xL, Mcl‐1, Bcl‐w and Bfl‐1, inhibit the mitochondrial pathway of apoptosis. Bcl‐xL and Mcl‐1 are constitutively expressed in the liver.

Hepatic targeting and biodistribution of human fetal liver stem/progenitor cells and adult hepatocytes in mice

Kang Cheng, Daniel Benten, Kuldeep Bhargava, Mari Inada, Brigid Joseph, Christopher Palestro, Sanjeev Gupta – 28 September 2009 – Tracking stem/progenitor cells through noninvasive imaging is a helpful means of assessing the targeting of transplanted cells to specific organs. We performed in vitro and in vivo studies wherein adult human hepatocytes and human fetal liver stem/progenitor cells were labeled with indium‐111 (111In)‐oxine and technetium‐99m (99mTc)‐Ultratag or 99mTc‐Ceretec.

Zinc supplementation reverses alcohol‐induced steatosis in mice through reactivating hepatocyte nuclear factor‐4α and peroxisome proliferator‐activated receptor‐α

Xinqin Kang, Wei Zhong, Jie Liu, Zhenyuan Song, Craig J. McClain, Y. James Kang, Zhanxiang Zhou – 28 September 2009 – Alcoholic steatosis is a fundamental metabolic disorder in the progression of alcoholic liver disease. Zinc deficiency is one of the most consistently observed biochemical/nutritional manifestations of alcoholic liver disease. The purpose of this study is to determine whether dietary zinc supplementation to mice previously exposed to alcohol could reverse alcoholic steatosis.

Subscribe to