Early endometriosis invades the extracellular matrix

Spuijbroek, Marleen D.E.H.; Dunselman, G.A.J.; Menheere, P. P. C. A.; Evers, Johannes L.H.

doi:10.1016/s0015-0282(16)55437-5

Cited by 143 publications

(63 citation statements)

References 17 publications

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“…10,11 It has been clearly shown that besides being responsible for the mass degradation of the ECM as bulldozers, matrix metalloproteinases (MMPs) play sophisticated roles in modulating normal cellular behavior and cell-cell communication, among which is the action of MMPs on cell growth through regulating several growth factors. 12 Several studies have shown an increase in the expression of MMP-1, MMP-2, MMP-3, MMP-7 and MMP-9 in endometriotic tissues.…”

Section: Introductionmentioning

confidence: 99%

Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells

Wang

Luo

et al. 2010

Cell Mol Immunol

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The chemokine thymus-expressed chemokine (TECK), which regulates T-cell development and tissue-specific homing, has been identified as a potential contributor to the pathogenesis and progression of endometriosis. Dioxin (2,3,7, TCDD), an air pollutant, and estrogen also appear to be involved in endometriosis. Both endometrial stromal cells (ESCs) and the combination of 17b-estradiol and TCDD increase the secretion of TECK in the endometriosis-associated cells and promote the invasiveness of ESCs by increasing expression of matrix metalloproteinase (MMP)-2 and MMP-9. Anti-TECK neutralizing antibodies can effectively inhibit the invasiveness of ESCs and the expression of MMP-2 and MMP-9 in the cells. Interestingly, the expression of chemokine C receptor 9 (CCR9) and its ligand TECK increases significantly in the endometriotic milieu of patients with endometriosis. Therefore, the over-expressed TECK interacts with CCR9 on the ESCs in the endometriotic milieu, which may contribute to the onset and progression of endometriosis.

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Section: Introductionmentioning

confidence: 99%

Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells

Wang

Luo

et al. 2010

Cell Mol Immunol

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“…Thus far, the pathogenesis of EM remains unclear, however, invasive mechanisms have been implicated in the development of this disease (21,22). The first tumor metastasis-suppressor gene, nm23, may be involved in the development of EM.…”

Section: Discussionmentioning

confidence: 99%

Association between nm23 gene polymorphisms and the risk of endometriosis

Huang

Zhao

et al. 2015

Biomedical Reports

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Abstract. The first tumor metastasis-suppressor gene, nm23, may have an important role in the pathogenesis of endometriosis (EM). The present study aimed to evaluate whether nm23 gene polymorphisms are correlated with the risk of the development of EM in North Chinese women, as a preliminary study. The case-control study was conducted with 379 EM patients and 384 unrelated healthy controls. Genotyping of two polymorphisms within the nm23 gene promoter region (rs16949649 T/C and rs2302254 C/T) were performed using polymerase chain reaction-restriction fragment length polymorphism. The data showed that the rs16949649 and rs2302254 polymorphisms within the nm23 gene were not associated with the risk of developing EM. There were no statistical differences in the distribution of nm23 genotypes between patients with EM and the control group (P= 0.490 and P= 0.440, respectively). For the rs16949649 T/C, compared with the C/T + T/T genotype, the C/C genotype did not increase the risk of EM [odds ratio (OR)= 0.81; 95% confidence interval (CI), 0.57-1.17]. For the rs2302254 C/T, compared with the C/T + C/C genotype, the T/T genotype did not increase the risk of EM (OR=1.46; 95% CI, 0.81-2.64). In conclusion, the findings in the present pilot study suggest that nm23 polymorphisms do not contribute to EM susceptibility. However, more studies in larger populations are required to confirm these results.

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“…Involvement of MMPs in endometriosis development was suspected after collagen breakdown products were found in the peritoneal fluid of patients with endometriosis (Spuijbroek et al, 1992) and since that time many studies have demonstrated that the pattern of MMPs expression in endometrium and peritoneal fluid of women with endometriosis significantly differ from that in healthy women (Nap et al, 2004). Increased levels of MMP-1, MMP-2, MMP-7 and MMP-9 were detected in peritoneal fluid of patients with endometriosis (Amalinie et al, 2010).…”

Section: Changes Of the Invasiveness Of Endometrium In Endometriosismentioning

confidence: 99%