Attachment to extracellular matrices is enhanced in human endometriotic stromal cells: a possible mechanism underlying the pathogenesis of endometriosis

Adachi, Masatake; Nasu, Kaei; Tsuno, Akitoshi; Yuge, Akitoshi; Kawano, Yukie; Narahara, Hisashi

doi:10.1016/j.ejogrb.2010.10.026

Cited by 35 publications

(31 citation statements)

References 38 publications

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“…Numerous studies have reported increased collagen content in endometriosis, [50][51][52] but collagen content in adenomyosis seems to have received scant attention. Eutopic and ectopic endometrial stromal cells derived from women with endometriosis possess stronger than normal endometrial stromal adhesion to ECM proteins such as collagen I and IV, 53,54 and selective inhibition of PTGER2-and PTGER4-mediated PGE 2 signaling decreases adhesion of endometriotic cells to collagen I, collagen IV and other ECM proteins. 55 The ECM proteins such as collagen IV may also promote proliferation of T cells 56 or induce apoptosis of the local immune cells including activated T lymphocytes, 57 facilitating the development of endometriosis.…”

Section: Discussionmentioning

confidence: 99%

“…The increased production may, in turn, further facilitate the development of adenomyosis by promoting proliferation and adhesion of ectopic endometrial stromal cells. 53,54 Since TGF-b1 is upregulated in mice with induced adenomyosis, 49 and since TGF-b1 is known to be a potent inducer of EMT in many tissues, 59 it is very likely that the stromal compartment of adenomyotic lesion would be enlarged, as in endometriosis, 60 which would facilitate the development of adenomyosis.…”

Section: Discussionmentioning

confidence: 99%

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Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

et al. 2014

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We have previously reported that induction of adenomyosis in mice results in progressive hyperalgesia, uterine hyperactivity, and elevated plasma corticosterone levels and that epigallocatechin-3-gallate (EGCG) treatment dose dependently suppressed myometrial infiltration and improved generalized hyperalgesia. In this study, we examined whether adenomyosis induced in mice results in the loss of GABAergic inhibition as manifested by the diminished glutamate decarboxylase (GAD) 65-expressing neurons in the brainstem nucleus raphe magnus (NRM) that could correlate with heightened hyperalgesia. We also evaluated whether EGCG treatment would reverse these changes and also improve the expression of some proteins known to be involved in adenomyosis. Adenomyosis was induced in 28 female ICR mice and additional 12 were used as blank controls, as reported previously. At the 16th week, all mice with induced adenomyosis received low-or high-dose EGCG treatment or untreated. Mice without adenomyosis received no treatment. After 3 weeks of treatment, their uterine horns and brains were harvested. The right uterine horn was used for immunohistochemistry analysis and for counting the number of macrophages infiltrating into the ectopic endometrium. The brainstem NRM sections were subjected to immunofluorescence staining for GAD65. We found that mice with induced adenomyosis had significantly diminished GAD65-expressing neurons, concomitant with heightened hyperalgesia. Treatment with EGCG increased these neurons in conjunction with improved hyperalgesia, reduced the expression of pp65, cycloxygenase 2, oxytocin receptor, collagen I and IV, and transient receptor potential vanilloid type 1 in ectopic endometrium or myometrium, reduced the number of macrophages infiltrating into the ectopic endometrium while elevated the expression of progesterone receptor isoform B. Thus, adenomyosis-induced pain resembles neuropathic pain in that there is a remarkable central plasticity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

et al. 2014

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“…Control endometrial tissues were obtained from 19 premenopausal patients who had undergone hysterectomies for subserosal leiomyoma without evidence of endometriosis, as described in a previous study (Adachi et al, 2011). All the women had abstained from medication for at least 3 months prior to donating the tissues.…”

Section: Endometriotic Tissues and Normal Controlsmentioning

confidence: 99%

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

Teng

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We examined the aberrant microRNA (miRNA) expression profile responsible for the changes in angiogenesis observed in endometriotic lesions. This study revealed characteristic miRNA expression profiles associated with endometriosis in endometrial tissue and endometriotic lesions from the same patient, and their correlation with the most important angiogenic and fibrinolytic factors. miRNA expression was quantified using a microRNA array and reversetranscription microRNA polymerase chain reaction. Levels of vascular endothelial growth factor A (VEGFA), epidermal growth factor receptor 2 (EGFR2), phosphatase and tensin homolog (PTEN), and C-X-C chemokine receptor type 4 (CXCR4) were quantified using enzyme-linked immunosorbent assay. The endometrial tissue showed significantly lower levels of miR-200b, miR-15a-5p, miR-19b-1-5p, miR-146a-5p, and miR-200c, and higher levels of miR-16-5p, miR106b-5p, and miR-145-5p. VEGFA was significantly upregulated, whereas EGFR2, PTEN, and CXCR4 were markedly downregulated, in the endometriotic tissues compared to that in the normal endometrial tissues. In conclusion, differences in the miRNA levels could modulate the expression of VEGFA, EGFR2, PTEN, and CXCR4, and may play an important role in the pathogenesis of endometriosis. The higher angiogenic and proteolytic activities observed in the eutopic endometrium might facilitate the implantation of endometrial cells at ectopic sites.

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“…These differences, such as reduced progesterone responsiveness, 8,13 increased resistance to apoptosis, 38 and increased cell adhesion capacity, 39 are considered to increase the survival of endometriotic tissues developed as a result of retrograde menstrual flux. In the current study, as far as the induction of CD10 by progesterone is concerned, we did not find any differences between the endometrial stromal cells associated with endometriosis and those not associated with endometriosis, although we demonstrated that there was a significant difference between endometrial stromal cells and endometriotic stromal cells.…”

Section: Discussionmentioning

confidence: 99%

Possible Involvement of CD10 in the Development of Endometriosis Due to Its Inhibitory Effects on CD44-Dependent Cell Adhesion

et al. 2014

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A reduced response to progesterone in the eutopic endometrium with endometriosis and in endometriotic tissues is considered to be the underlying factor for endometriosis. CD10 is known to be expressed by endometrial and endometriotic stromal cells and may be induced by progestins, although the function of CD10 is not fully revealed in endometrial or endometriotic tissues. In the current study, the expression of CD10 was significantly increased by treatment of the cells with progesterone, 17b-estradiol, and dibutyryl cyclic adenosine monophosphate (cAMP) in the endometrial stromal cells. On the other hand, the expression of CD10 following treatment with progesterone, 17b-estradiol, and dibutyryl cAMP was not significantly increased in endometriotic stromal cells. The adhesion assay for endometrial and endometriotic stromal cells to hyaluronan using 5-or 6-(N-succinimidyloxycarbonyl)-fluorescein 3', 6'-diacetate-labeled cells demonstrated that the CD44-dependent adhesion of stromal cells was inhibited by CD10. As far as the induction of CD10 is concerned, the effect of progesterone was different between endometrial stromal cells and endometriotic stromal cells. CD10 might be involved in the development of endometriosis due to its influence on CD44-dependent cell adhesion.

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Attachment to extracellular matrices is enhanced in human endometriotic stromal cells: a possible mechanism underlying the pathogenesis of endometriosis

Cited by 35 publications

References 38 publications

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

Possible Involvement of CD10 in the Development of Endometriosis Due to Its Inhibitory Effects on CD44-Dependent Cell Adhesion

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