[Histological analysis of spontaneous adenomyosis-like changes in recombinant inbred mouse uterus (SMXA mouse)--a novel animal model for adenomyosis].
The etiology and the pathogenesis of adenomyosis, which is a benign uterine disease featuring the ectopic proliferation of endometrial tissues and glands into the myometrium and the serosa in the uterus, are still unknown. A novel mouse strain, which showed signs of a condition resembling adenomyosis, was found and the localization of alpha-actin and tenascin was analyzed in order to characterize the histological features of this disease. 1. The uteri of recombinant inbred SMXA mice were shown to have undergone spontaneous histological changes similar to adenomyosis. 2. Compared with SMXA mice, the uteri of F1 mice between the SMXA and NJL strains showed further prominent changes resembling human adenomyosis, which suggests that some hereditary factors may be involved in the pathogenesis of adenomyosis. 3. In a normal mouse uterus, the regions in which tenascin was expressed change with the estrus cycle. In SMXA mice, tenascin was expressed around the dysplastic and cystic uterine glands, and in the myometrium. These results indicated that tenascin is an important marker of the histological changes in adenomyosis. 4. SMXA mice, which are recombinant inbred mice, are shown to be a useful animal model to use in analyzing the pathogenetic mechanisms of adenomyosis.