A subpopulation of bone marrow cells depleted by a novel antibody, anti-Liv8, is useful for cell therapy to repair damaged liver.
A subpopulation of bone marrow cells depleted by a novel antibody, anti-Liv8, is useful for cell therapy to repair damaged liver.
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DOI：
10.1016/j.bbrc.2003.12.044
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发表时间：
2004-01
影响因子：
3.1
通讯作者：
N. Yamamoto;S. Terai;Shinya Ohata;Tomomi Watanabe;K. Omori;K. Shinoda;K. Miyamoto;T. Katada;I. Sakaida;H. Nishina;K. Okita
中科院分区：
文献类型：
--
作者：
N. Yamamoto;S. Terai;Shinya Ohata;Tomomi Watanabe;K. Omori;K. Shinoda;K. Miyamoto;T. Katada;I. Sakaida;H. Nishina;K. Okita
我们以前报道了一种新的体内模型，命名为GFP/CCl4模型，用于监测在CCl4诱导的持续性肝损伤的特定生态位下，绿色荧光蛋白(GFP)阳性的骨髓细胞(BMC)向白蛋白阳性肝细胞的转分化，但BMC转分化为肝细胞的亚群尚不清楚。本文以小鼠E11.5胎肝为抗原，研制了一种新的单抗--抗Liv8。抗Liv8抗体可识别胚胎肝脏E11.5位造血祖细胞和成人骨髓CD45阳性造血细胞。我们分离了Liv8阳性细胞和Liv8阴性细胞，然后将这些细胞移植到持续肝损伤模型中。在BMC移植后4周，Liv8阴性细胞的BMC向肝细胞的再分化和转分化更为有效。这些发现表明，Liv8阴性细胞亚群中包括对修复受损肝脏进行细胞治疗的有用细胞。
We previously reported a new in vivo model named as “GFP/CCl4model” for monitoring the transdifferentiation of green fluorescent protein (GFP) positive bone marrow cell (BMC) into albumin-positive hepatocyte under the specific “niche” made by CCl4induced persistent liver damage, but the subpopulation which BMCs transdifferentiate into hepatocytes remains unknown. Here we developed a new monoclonal antibody, anti-Liv8, using mouse E 11.5 fetal liver as an antigen. Anti-Liv8 recognized both hematopoietic progenitor cells in fetal liver at E 11.5 and CD45-positive hematopoietic cells in adult bone marrow. We separated Liv8-positive and Liv8-negative cells and then transplanted these cells into a continuous liver damaged model. At 4 weeks after BMC transplantation, more efficient repopulation and transdifferentiation of BMC into hepatocytes were seen with Liv8-negative cells. These findings suggest that the subpopulation of Liv8-negative cells includes useful cells to perform cell therapy on repair damaged liver.