Changes in Uterine Microvessels as a Possible Pathogenic Factor in the Development of Adenomyosis Induced by Pituitary Grafting in Mice.

Zhou, Yang; Matsuda, Manabu; Sakamoto, Shinobu; Mori, Taketoshi

doi:10.1267/ahc.32.387

Cited by 6 publications

(2 citation statements)

References 17 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The histological features of the adenomyosis in this present study using this 5-day treatment regimen of SERMs possessed the histological features described previously both in animal models and in humans. 1,11,12 Moreover, this was produced without the confounding effects of surgical trauma of the mouse pituitary implantation model. Nodules of endometrial glands and stroma were present deep within the myometrium, sometimes extending to, but not penetrating, the serosa.…”

Section: Discussionmentioning

confidence: 99%

Adenomyosis—A Result of Disordered Stromal Differentiation

Parrott

Butterworth

Green

et al. 2001

The American Journal of Pathology

126

111

View full text Add to dashboard Cite

Adenomyosis is a fairly frequent disorder in adult women characterized by the haphazard location of endometrial glands and stroma deep within the myometrium of the uterus. This study compared the effects on uterine development of the selective estrogen receptor modulators, tamoxifen, toremifene, and raloxifene with estradiol when given orally to female mice on days 2 to 5 after birth. Uterine adenomyosis was found in all (14 of 14) mice dosed with tamoxifen and most mice (12 of 14) treated with toremifene, but in none of the vehicle-dosed controls, in only one animal treated with raloxifene at 42 and 90 days after dosing and in none of the mice treated with estradiol at 42 days. At 6 days, the uterus in the groups that developed a high incidence of adenomyosis showed histological evidence of disturbed differentiation of the myometrium. Gene-expression XY-scatterplots using Clontech mouse 1.2 Atlas mouse cDNA expression arrays analyzing total uterine RNA showed nerve growth factor-alpha, preadipocyte factor-1, and insulin-like growth factor-2 were key genes differentially modified by tamoxifen or toremifene treatment, relative to the controls. As these genes may play an important role in regulating differentiation and development of the myometrium, these data suggest that adenomyosis may be caused primarily by defects in the formation of the myometrium.

show abstract

Section: Discussionmentioning

confidence: 99%

Adenomyosis—A Result of Disordered Stromal Differentiation

Parrott

Butterworth

Green

et al. 2001

The American Journal of Pathology

126

111

View full text Add to dashboard Cite

show abstract

“…In the development of adenomyosis induced by PG grafting. an early sign of the disorder is the invasion of stromal fibroblasts into the myometrium along the branches of blood vessels (7)(8)(9)(10). Disintegration of muscular bundles of the inner myometrium due to derangement and involution of muscle cells associated with widening of intercellular spaces appears to facilitate the invasion of stromal cells (9.…”

Section: U Terine Adenom~osismentioning

confidence: 99%

Suppression of the Development of Experimentally Induced Uterine Adenomyosis by a Novel Matrix Metalloproteinase Inhibitor, ONO-4817, in Mice

Mori

Yamasaki

Masui

et al. 2001

Exp Biol Med (Maywood)

Self Cite

View full text Add to dashboard Cite

The inhibitory effects of a novel, orally active matrix metalloproteinase (MMP) inhibitor, ONO-4817, on the development of uterine adenomyosis induced experimentally by pituitary grafting were examined in mice. Mice were given transplants of isologous anterior pituitary glands (PGs) into the right uterine lumen at 7 weeks of age and were fed chow containing 0.1% to 1.0% ONO-4817 from 8 to 14 weeks of age. Mice treated with 0.3% or 1.0% ONO-4817 showed a significantly lower incidence of the development of adenomyosis than vehicle-treated mice. To evaluate the inhibitory effects of ONO-4817 on the progression of the invasion of the adenomyotic tissues, mice receiving PG grafts at 7 weeks of age were treated with 1.0% ONO-4817 from 13 to 17 weeks of age. The degree of pathological progression of adenomyosis was graded from 1 to 5 in increments of 1. The degree of the progression of the lesion was less in the uteri exposed to ONO-4817 (2.71 ± 0.93) than in the uteri not exposed to the inhibitor (4.33 ± 0.75). Finally, the invasiveness of endometrial stromal cells obtained from adenomyotic uteri into Matrigel consisting mainly of type IV collagen and laminin was examined using an invasion assay. The assay showed that the treatment with ONO-4817 markedly suppressed the invasion of the stromal cells of the adenomyotic uteri into the gel. These results indicate that ONO-4817 may be an effective inhibitor of the development of adenomyosis.

show abstract