Histochemical Analysis Using Lectin in the Mouse Uterine Tissues with Experimentally-Induced Adenomyosis.

Haruko Sasabe, Manabu Matsuda, Takao Mori
In: ACTA HISTOCHEMICA ET CYTOCHEMICA · 1998 · vol. 31(2) , pp. 105–112 · doi:10.1267/ahc.31.105 · W2054349709
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Histochemical analysis of experimentally-induced adenomyosis in mice revealed distinct lectin staining patterns in glandular epithelial cells, luminal epithelial cells, and lymphocytes compared to intact controls, with some changes mirroring those seen post-parturition.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

The study examined mouse uterine tissues using histochemical lectin staining, comparing control uteri from intact mice and mice one day after parturition with uteri from mice that developed experimentally induced adenomyosis via transplantation of a single anterior pituitary into the uterine lumen, which caused hyperprolactinemia. Using 21 biotinylated lectins, the authors found that lectin binding patterns differed between adenomyotic and control uteri specifically in glandular and luminal epithelial cells and lymphocytes, while endometrial stromal cells and myometrial cells showed no differences. They also reported that even at very early stages of adenomyosis, lectin binding patterns already changed, with some lectins resembling post-delivery patterns (linked to elevated circulating prolactin) and others differing in ways tied to adenomyosis pathology. This paper is centrally about adenomyosis — it uses lectin histochemistry to characterize early molecular/biochemical changes in an experimentally induced mouse model of adenomyosis.

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Abstract

Transplantation of a single anterior pituitary into the uterine lumen is known to induce the development of adenomyosis in mice associated with hyperprolactinemia. The uterine tissues of experimentally-induced adenomyosis were investigated histochemically with 21 kinds of biotinylated lectins and compared to control tissues of both intact mice and mice one day after parturition. Glandular and luminal epithelial cells and lymphocytes showed different lectin staining patterns between adenomyotic uteri and intact ones, whereas endometrial stromal cells and myometrial cells showed no differences. Even uteri at a very early stage of the pathological disorder already had changes in their lectin binding pattern. Some lectin groups had a different staining pattern between adenomyotic uteri and intact ones. Among them, some showed a similar pattern between adenomyotic uteri and uteri after delivery, and the others showed a different pattern between them. The former groups were closely related to an elevated level of circulating prolactin, and the latter to a pathological change in adenomyosis. This is the first evidence which shows that experimentally-induced adenomyosis involves substantial changes even at a very early stage of the pathogenesis.

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adenomyosis

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