Background Lesions during a 24-Month Observation Period in Connexin 32-Deficient Mice

Connexin 32 (Cx32) is a major gap junction protein in the liver. Neoplastic and non-neoplastic lesions were examined in Cx32-deficient (Cx32KO) mice maintained for 24-month, and compared with those in wild-type mice as a corresponding control. In neoplastic lesions, hepatocellular carcinoma increase...

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Bibliographic Details
Published in:Journal of Veterinary Medical Science 2013, Vol.75(2), pp.207-210
Main Authors: IGARASHI, Isao, MAKINO, Toshihiko, SUZUKI, Yoko, KAI, Kiyonori, TERANISHI, Munehiro, TAKASAKI, Wataru, FURUHAMA, Kazuhisa
Format: Article
Language:English
Subjects:
Adenoma - genetics
Adenoma - metabolism
Adenoma - pathology
Animals
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
connexin 32
Connexins - genetics
Connexins - metabolism
Female
Gap Junction beta-1 Protein
Gene Expression Regulation - physiology
Genetic Predisposition to Disease
intercellular communication
knock-out mice
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Mice
Mice, Knockout
Pituitary Neoplasms - genetics
Pituitary Neoplasms - metabolism
Pituitary Neoplasms - pathology
Sex Factors
spontaneous mass
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Summary:Connexin 32 (Cx32) is a major gap junction protein in the liver. Neoplastic and non-neoplastic lesions were examined in Cx32-deficient (Cx32KO) mice maintained for 24-month, and compared with those in wild-type mice as a corresponding control. In neoplastic lesions, hepatocellular carcinoma increased significantly only in male Cx32KO mice, suggesting that Cx32 deficiency may be related to their pathogenesis. For females, the incidence of pituitary adenoma in the pars distalis of Cx32KO mice was lower than that of wild-type mice. No non-neoplastic lesions related to Cx32-deficiency were observed in the Cx32KO mice. In conclusion, these results demonstrate that the incidence of hepatocellular carcinoma increases only in male Cx32KO mice, presumably due to enhanced tumor promotion and progression signals associated with Cx32 deficiency.
ISSN:0916-7250
1347-7439
DOI:10.1292/jvms.12-0280