抗コネクシソ32, 26抗体を用いたラット肝Gap Junctionの免疫組織化学的研究 : 特に発生・再生・発癌過程における変化について

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  • Immunohistochemical Studies of Gap Junction in the Rat Liver with Anti-CX26 and Anti-CX32 Antibodies : Distributional Changes of CX32 and CX26 in the Rat Liver in the Developmental, Regenerating and Hepatocarcinogenic Stages

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Gap junctions are channels through which ions and small molecules are directly exchanged between adjacent cells, and consist of connexon. Connexon is composed of 6 connexin （CX） molecules, of which CX32 and CX26 have been isolated from the rat liver. To study distributional changes of CX32 and CX26 in rat hepatocytes in the developmental, regenerating and carcinogenic processes, we performed immunohistochemical analysis using a new polyclonal antibody, anti-CX26 antibody, and an antibody which we reported on previously, anti-CX32 antibody, both raised against synthetic peptides of the intracytoplasmic domain. With liver maturation, the CX32 positive-spots （CX32-PS） remained evenly distributed throughout the acinus of the liver and increased in number. However the CX26-PS, which were sparsely distributed in the embryonic stage, became localized specifically in the periportal area without an increase in number. Thus, we suppose that the alteration of localization of CX26 might be associated with maturation of the liver. In rat livers regenerating after partial hepatectomy, changes in the number of CX26-PS were similar to those of CX32-PS. This result suggests that these CXs might be controlled by the same mechanism. In preneoplastic lesions induced by the method of Solt and Farber, the number of CX32-PS decreased, whereas the number of CX26-PS increased in about half of the lesions. In hepatocellular carcinomas, the numbers of both CX26- and CX32-PS decreased. These results suggest that the expression of CX32 and CX26 might be regulated differently during hepatocarcinogenesis. CX32 and CX26 mostly showed similar patterns in the immunofluorescent study. In preneoplastic lesions, however, the two CXs showed obvious differences in their numbers. The significance of the quantitative changes of gap junctions during hepatocarcinogenesis has yet to be investigated.

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