Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-3 mRNA expression in ectopic and eutopic endometrium in women with endometriosis: a rationale for endometriotic invasiveness

Chung, Hye Won; Wen, Yan; Sun, Chun; Nezhat, Camran; Woo, Bock Hi; Polan, Mary Lake

doi:10.1016/s0015-0282(00)01670-8

Cited by 168 publications

(119 citation statements)

References 27 publications

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“…In addition, MMPs expression appeared to be involved in the implantation of endometrial tissues since the establishment of ectopic endometriotic lesions failed when MMPs secretion was blocked (Bruner et al 1997). In the same way, it has been reported that MMP-2 (Wenzl & Heinzl 1998) and MMP-9 expression was increased in endometriotic lesions (Chung et al 2001). In the present study, we found that MMP-2 and MMP-9 secretion was increased in the A clones in response to IL1B.…”

Section: Stable Inhibition Of Il1r2supporting

confidence: 80%

“…In women with endometriosis, several studies showed an increased expression in ectopic and eutopic endometrial tissues of several proteases including MMPs (Bergqvist et al 1996, Chung et al 2001, Bruse et al 2004, Collette et al 2004, 2006. These enzymes have been involved in the invasive establishment of the disease (Gilabert-Estelles et al 2003, Osteen et al 2003.…”

Section: Stable Inhibition Of Il1r2mentioning

confidence: 99%

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Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

Guay

Akoum²

2007

Reproduction

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Our previous studies showed a marked deficiency in interleukin 1 receptor type II (IL1R2) in the endometrial tissue of women with endometriosis, particularly in epithelial cells. We believe that such a deficiency in IL1R2, a potent and specific IL1 inhibitor, makes endometrial cells more sensitive to IL1 and less capable of buffering the cytokine's effects, which may lead to functional changes that favor endometriosis development. The main objective of our study was to stably inhibit IL1R2 expression in endometrial cells in order to evaluate the role of IL1R2 deficiency in endometriosis pathophysiology. Stable clones of Ishikawa adenocarcinoma endometrial cells transfected with IL1R2 antisense and showing downregulation of IL1R2 protein expression, or with the empty expression vector alone and showing no noticeable difference in IL1R2 expression, were selected. The downregulation of IL1R2 expression in IL1R2 antisense transfectants when compared with control cells was confirmed by ELISA, Western blot and immunofluorescence. In these cells, IL1R2 expression was markedly reduced, compared with non-transfected cells or cells transfected with the empty vector, and there was a significant increase in the basal and the IL1-b (IL1B)-induced levels of matrix metalloproteinase (MMP)-2 and MMP-9 secretion. Furthermore, a significant decrease in IL1B-induced secretion of tissue inhibitor of MMPs-1, a known MMP-9 inhibitor, was observed. These in vitro data make plausible a role for IL1R2 deficiency in the capability of endometrial cells to invade the host tissue and develop in ectopic locations. Reproduction (2007) 134 525-534

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Section: Stable Inhibition Of Il1r2supporting

confidence: 80%

Section: Stable Inhibition Of Il1r2mentioning

confidence: 99%

Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

Guay

Akoum²

2007

Reproduction

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“…In endometriotic lesions, ICAM1 is released from the cell membrane by proteolytic cleavage of its extracellular domain, with a parallel increase in expression and proteolytic activity of certain MMPs, including MMP1 and MMP9 (Vigano et al 1998, Chung et al 2001, Mizumoto et al 2002, Hudelist et al 2005. MMP1 shows altered levels in culture supernatants of uterine endometrial cells from patients with endometriosis compared with the endometria from healthy women (Sillem et al 2001), and a positive correlation between its altered secretion and the development and activity of endometriotic foci has been described (Kokorine et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Pino¹,

Galleguillos²,

Torres³

et al. 2009

Reproduction

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Endometriosis is a benign gynecological pathology in which immune system deregulation may play a role in its initiation and progression. In endometriotic lesions, intercellular adhesion molecule-1 (ICAM1) is released from the cell membrane by proteolytic cleavage of its extracellular domain, a process that coincides with increased expression and proteolytic activity of metalloproteinases such as MMP1 and MMP9. The objective of our study was to investigate the association between MMP1 and MMP9 activities and ICAM1 cleavage mediated by tumor necrosis factor (TNF) in eutopic endometrial stromal cells from women with and without (control) endometriosis during culture. The RNA was evaluated by RT-PCR, and the protein was determined by western blot (ICAM1, MMP1), casein or gelatin zymographies (secreted active MMP1 or MMP9 respectively), ELISA (soluble ICAM1 (sICAM1)), and fluorescence assay (secreted active MMP1). Under basal conditions, proMMP9 dimer and MMP9 were higher in endometriosis cell cultures. In stromal cultures derived from control women and those with endometriosis, TNF augmented the intracellular proMMP1 (1.2-fold in control stromal cells) and ICAM1 (1.4-and 1.9-fold), greatly increased MMP1 and proMMP9 levels, and the sICAM1 concentration (2.3-and 4.3-fold) in their media compared with basal levels. The combination of TNF and MMP9 increased the sICAM1 concentration 14-fold in the endometriosis cell media, whereas GM6001 inhibited the stimulatory effect of TNF in both cell cultures. The deregulation of MMP9, and the TNF participation in the MMP1 and proMMP9 secretions, in the MMP9 expression and in the expression and cleavage of ICAM1 may contribute to the pathophysiology of this disease.

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“…Expression of matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) is reportedly involved in the pathogenesis and pathophysiologies of endometriosis occurring in women and in animal models [17][18][19][20][21][22]. The MMPs are a family of enzymes that degrade the extracellular matrix, including basement membrane components [23].…”

Section: Introductionmentioning

confidence: 99%

Proteasomes and Proteasome Activator 200 kDa (PA200) Accumulate on Chromatin in Response to Ionizing Radiation

Blickwedehl¹,

McEvoy²,

Wong³

et al. 2007

Radiation Research

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Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-3 mRNA expression in ectopic and eutopic endometrium in women with endometriosis: a rationale for endometriotic invasiveness

Cited by 168 publications

References 27 publications

Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Proteasomes and Proteasome Activator 200 kDa (PA200) Accumulate on Chromatin in Response to Ionizing Radiation

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