Increase in the number of integrinbeta1-immunoreactive monocyte-lineage cells in experimentally-induced adenomyosis in mice.

Uterine adenomyosis is a disease in which hyperplastic endometrial stroma and glands invade the myometrium. We have previously demonstrated that hyperprolactinemia leads to the development of adenomyosis in mice. In the present study, a subtracted cDNA library was made by suppression subtractive hybridization to find specific genes that are abundantly expressed in the adenomyotic but not normal tissue in mice. A cDNA fragment of integrinbeta1 (ibeta1) was found in the library, and the expression of the gene product was increased in the adenomyotic uteri at mRNA and protein levels. Intense ibeta1-immunoreactivity was localized on a group of cells dispersing throughout the endometrial stroma. The number of ibeta1-immunoreactive (ibeta1-ir) cells was significantly greater in the uteri of mice with adenomyosis than normal mice. The majority of the ibeta1-ir cells expressed CD14-ir signal, a marker for monocyte-lineage cells, whereas an increase in the number of CD14-ir cells was also evident in the adenomyotic uteri, especially in the ectopic endometrial tissue. Thus, the adenomyotic stromal tissue contained numerous monocyte-lineage cells with higher expression levels of ibeta1, one of their products. The relationship between the increased number of monocyte-lineage cells and the hyperplastic proliferation of endometrial tissues was discussed with a view to understanding the progressive mechanism of adenomyosis.