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  1. Article: Mechanobiology of the female reproductive system.

    Matsuzaki, Sachiko

    Reproductive medicine and biology

    2021  Volume 20, Issue 4, Page(s) 371–401

    Abstract: Background: Mechanobiology in the field of human female reproduction has been extremely challenging technically and ethically.: Methods: The present review provides the current knowledge on mechanobiology of the female reproductive system. This ... ...

    Abstract Background: Mechanobiology in the field of human female reproduction has been extremely challenging technically and ethically.
    Methods: The present review provides the current knowledge on mechanobiology of the female reproductive system. This review focuses on the early phases of reproduction from oocyte development to early embryonic development, with an emphasis on current progress.
    Main findings results: Optimal, well-controlled mechanical cues are required for female reproductive system physiology. Many important questions remain unanswered; whether and how mechanical imbalances among the embryo, decidua, and uterine muscle contractions affect early human embryonic development, whether the biomechanical properties of oocytes/embryos are potential biomarkers for selecting high-quality oocytes/embryos, whether mechanical properties differ between the two major compartments of the ovary (cortex and medulla) in normally ovulating human ovaries, whether durotaxis is involved in several processes in addition to embryonic development. Progress in mechanobiology is dependent on development of technologies that enable precise physical measurements.
    Conclusion: More studies are needed to understand the roles of forces and changes in the mechanical properties of female reproductive system physiology. Recent and future technological advancements in mechanobiology research will help us understand the role of mechanical forces in female reproductive system disorders/diseases.
    Language English
    Publishing date 2021-07-31
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 2185775-1
    ISSN 1447-0578 ; 1445-5781
    ISSN (online) 1447-0578
    ISSN 1445-5781
    DOI 10.1002/rmb2.12404
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  2. Article ; Online: Impaired secretion of C-X-C motif chemokine ligand 10 by stimulation with a Toll-like receptor 4 ligand in endometrial epithelium of infertile patients with minimal-to-mild endometriosis.

    Matsuzaki, Sachiko / Chauffour, Candice / Pouly, Jean-Luc

    Journal of reproductive immunology

    2023  Volume 159, Page(s) 103989

    Abstract: Successful embryo implantation requires transient, well-controlled inflammation in decidualizing cells. In mice, Toll-like receptor (TLR) 4 signaling in endometrial epithelial cells (EECs) by stimulation with factors present in seminal fluids has been ... ...

    Abstract Successful embryo implantation requires transient, well-controlled inflammation in decidualizing cells. In mice, Toll-like receptor (TLR) 4 signaling in endometrial epithelial cells (EECs) by stimulation with factors present in seminal fluids has been shown to be a key upstream driver of a controlled inflammatory response. Clinical evidence supports that exposure of the female reproductive tract to seminal plasma promotes implantation success. We investigated the response of EECs to TLR2 (Pam3Csk4), TLR 3 (Poly I:C), and TLR4 (lipopolysaccharides [LPS]) ligands with respect to secretion of C-X-C motif chemokine ligand (CXCL) 10 (CXCL10) and interleukin-6 (IL-6) in infertile patients with minimal-to-mild endometriosis (EECs-endo) (n = 38) and those of healthy, fertile women (EECs-healthy) (n = 30). Stimulation with either Pam3Csk4, Poly I:C or LPS, significantly induced CXCL10 and IL-6 in EECs-healthy (p < 0.05). In EECs-endo, either Pam3Csk4 or Poly I:C significantly induced CXCL10 (p < 0.05), whereas no significant response was observed after stimulation with LPS. Neither LPS, Poly I:C, nor Pam3Csk4 significantly induced IL-6 secretion in EECs-endo. Secretion of CXCL10 in EECs-healthy after stimulation with LPS was significantly higher (p < 0.05) than that in EECs-endo. CXCL10 decreased cell proliferation of EECs from both groups. Activation of nuclear factor kappa light chain enhancer of activated B cells and signal transducer and activator of transcription 3 signalings was not impaired, but activation of p38 mitogen-activated protein kinases signaling by LPS stimulation was impaired in EECs-endo. The present findings suggested that an insufficient response of EECs to a TLR4 ligand may be involved in molecular mechanisms of endometriosis-associated infertility.
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Endometriosis/complications ; Epithelium ; Interleukin-6 ; Ligands ; Lipopolysaccharides/pharmacology ; Poly I ; Toll-Like Receptor 4/metabolism ; Infertility, Female/etiology
    Chemical Substances Interleukin-6 ; Ligands ; Lipopolysaccharides ; Poly I (25249-22-3) ; Toll-Like Receptor 4
    Language English
    Publishing date 2023-07-11
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 424421-7
    ISSN 1872-7603 ; 0165-0378
    ISSN (online) 1872-7603
    ISSN 0165-0378
    DOI 10.1016/j.jri.2023.103989
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  3. Article ; Online: IL-10 is not anti-fibrotic but pro-fibrotic in endometriosis: IL-10 treatment of endometriotic stromal cells in vitro promotes myofibroblast proliferation and collagen type I protein expression.

    Matsuzaki, Sachiko / Pouly, Jean-Luc / Canis, Michel

    Human reproduction (Oxford, England)

    2022  Volume 38, Issue 1, Page(s) 14–29

    Abstract: Study question: Is interleukin-10 (IL-10) anti-fibrotic in endometriosis?: Summary answer: IL-10 is not anti-fibrotic but pro-fibrotic in endometriosis, because IL-10 treatment of endometriotic stromal cells in vitro promotes myofibroblast ... ...

    Abstract Study question: Is interleukin-10 (IL-10) anti-fibrotic in endometriosis?
    Summary answer: IL-10 is not anti-fibrotic but pro-fibrotic in endometriosis, because IL-10 treatment of endometriotic stromal cells in vitro promotes myofibroblast proliferation and collagen type I protein expression.
    What is known already: We previously showed that persistent activation of signal transducer and activator of transcription 3 (STAT3) via IL-6 trans-signaling promotes fibrosis of endometriosis. Studies showed marked anti-fibrotic effects of IL-10 via the STAT3 signaling pathway, which is generally considered to be anti-inflammatory, in various organs.
    Study design, size, duration: Endometrial and/or endometriotic samples of 54 patients who had histological evidence of deep endometriosis, and endometrial samples from 30 healthy fertile women were analyzed.
    Participants/materials, setting, methods: The effects of IL-10/STAT3 signaling as well as inhibition of STAT3 activation by knockdown of STAT3 gene on the pro-fibrotic phenotype in endometrial and endometriotic stromal cells in vitro were investigated. Then, the effects of various time points of IL-10 treatment in combination with transforming growth factor (TGF)-β1 and/or IL-6/soluble IL-6 receptor (sIL-6R) on the profibrotic phenotype of endometrial and endometriotic stromal cells were investigated.
    Main results and the role of chance: IL-10 induced pro-fibrotic phenotype (cell proliferation, collagen type I synthesis, α-smooth muscle actin positive stress fibers and collagen gel contraction) of endometriotic stromal cells. Knockdown of STAT3 gene decreased the IL-10 induced pro-fibrotic phenotype of endometriotic stromal cells. In contrast, IL-10 had no significant effects on pro-fibrotic phenotype of endometrial stromal cells of healthy women. Sequential IL-10 treatment with or without TGF-β1 and/or IL-6/sIL-6R induced persistent activation of STAT3 and significantly increased proliferation of myofibroblasts (cells with α-smooth muscle actin positive stress fibers) and protein expression of collagen type I in endometriotic stromal cells. TGF-β1 and/or IL-6/sIL6RIL-6/sIL6R treatment significantly increased tissue inhibitor of metalloproteinase 1 (TIMP1) protein expression, whereas IL-10 had no significant effects. Knockdown of STAT3 gene significantly decreased the TGF-β1 and/or IL-6/sIL6R induced TIMP1 protein expression. In contrast, pre-treatment with IL-10 before TGF-β1 and/or IL-6/sIL-6R treatment and sequential IL-10 treatment with or without TGF-β1 and/or IL-6/sIL-6R significantly decreased proliferation of fibroblasts (cells without α-smooth muscle actin positive stress fibers) and collagen type I protein expression in endometrial stromal cells of healthy women.
    Large scale data: N/A.
    Limitations, reasons for caution: Given the large number of complex interactions and signaling pathways of pro- and anti-inflammatory mediators that are involved in the pathophysiology of endometriosis, the present study investigated only a very small portion of the whole. Further in vivo studies are required to validate the present findings.
    Wider implications of the findings: Inflammatory mediators in the pathophysiology of endometriosis have been extensively investigated as potential therapeutic targets. However, the present study showed that anti-inflammatory signals of IL-10 and IL-6 through persistent STAT3 activation may promote endometriosis fibrosis. Therapeutic strategies, such as suppression of 'inflammation', might dysregulate the cross-regulation of 'pro- and anti-inflammatory mediators', leading to detrimental effects in patients with endometriosis, such as fibrosis. To develop new, but not deleterious, therapeutic strategies, studies are required to investigate whether, how and what 'anti-inflammatory mediators' along with pro-inflammatory mediators are involved in individual patients with endometriosis.
    Study funding/competing interest(s): This study was supported in part by KARL STORZ SE & Co. KG (Tuttlingen, Germany). The authors have no conflict of interest to disclose.
    MeSH term(s) Humans ; Female ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Myofibroblasts/metabolism ; Transforming Growth Factor beta1/metabolism ; Interleukin-10/metabolism ; Actins/metabolism ; Endometriosis/metabolism ; Interleukin-6/metabolism ; Tissue Inhibitor of Metalloproteinase-1/metabolism ; Stromal Cells/metabolism ; Cell Proliferation ; Fibrosis ; Endometrium/metabolism
    Chemical Substances Collagen Type I ; Transforming Growth Factor beta1 ; Interleukin-10 (130068-27-8) ; Actins ; Interleukin-6 ; Tissue Inhibitor of Metalloproteinase-1
    Language English
    Publishing date 2022-12-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632776-x
    ISSN 1460-2350 ; 0268-1161 ; 1477-741X
    ISSN (online) 1460-2350
    ISSN 0268-1161 ; 1477-741X
    DOI 10.1093/humrep/deac248
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Persistent activation of signal transducer and activator of transcription 3 via interleukin-6 trans-signaling is involved in fibrosis of endometriosis.

    Matsuzaki, Sachiko / Pouly, Jean-Luc / Canis, Michel

    Human reproduction (Oxford, England)

    2022  Volume 37, Issue 7, Page(s) 1489–1504

    Abstract: Study question: Is activation of signal transducer and activator of transcription 3 (STAT3) via interleukin-6 (IL-6) trans-signaling involved in fibrosis of endometriosis?: Summary answer: Persistent activation of STAT3 via IL-6 trans-signaling is ... ...

    Abstract Study question: Is activation of signal transducer and activator of transcription 3 (STAT3) via interleukin-6 (IL-6) trans-signaling involved in fibrosis of endometriosis?
    Summary answer: Persistent activation of STAT3 via IL-6 trans-signaling is involved in fibrosis of endometriosis.
    What is known already: Our previous study showed that sustained low-grade inflammation promotes a fibrotic phenotype in endometriotic stromal cells. However, the underlying mechanisms of the establishment of non-resolving, low-grade inflammation in endometriosis remain to be clarified.
    Study design, size, duration: Endometrial and/or endometriotic samples of 60 patients who had histological evidence of deep endometriosis and endometrial samples from 32 healthy fertile women were analyzed.
    Participants/materials, setting, methods: The effects of priming with ligands of Toll-like receptors (TLRs) 2, 3 and 4 on secretion of inflammatory mediators (tumor necrosis factor-α, C-X-C motif chemokine ligand-10 [CXCL-10], IL6 and IL-10) after a second challenge with TLR ligands in endometrial and endometriotic stromal cells were investigated. Then, the effects of IL-6/soluble (s) IL-6 receptor (R)/STAT3 signaling, as well as inhibition of STAT3 activation by knockdown of STAT3 or pharmacological inhibition (S3I-201), on the pro-fibrotic phenotype in endometrial and endometriotic stromal cells in vitro were investigated.
    Main results and the role of chance: Priming with TLR ligands for 4 h had no significant effects, whereas 24 h of priming significantly decreased secretion of IL-6, after a second challenge in endometrial stromal cells of healthy women. In endometriotic stromal cells, whereas 24 h of priming had no significant effects, priming with TLR ligands for 4 h significantly increased secretion of IL-6 after a second challenge. IL-6/soluble IL-6 receptor (sIL-6R) induced a pro-fibrotic phenotype (cell proliferation, collagen type I synthesis, α-smooth muscle actin positive stress fibers, cell migration and collagen gel contraction) as well as nuclear factor-kappa B (NF-κB) activation of endometriotic stromal cells. In contrast, IL-6/sIL-6R had no significant effects on either a pro-fibrotic phenotype or NF-κB activation of endometrial stromal cells of healthy women. Stimulation with transforming growth factor (TGF)-β1 and/or IL-6/sIL-6R for 1 h and 48 h activated STAT3, but induced very low or no suppressor of cytokine signaling (SOCS) 1 and 3 protein expression in endometriotic stromal cells. In endometrial stromal cells of healthy women, IL-6/sIL-6R-induced STAT3 and SOCS1/3 expression at 1 h, whereas no STAT3 activation was detected at 48 h. Knockdown of STAT3 gene or S3I-201 (a STAT3 inhibitor) decreased the IL-6/sIL-6R-induced pro-fibrotic phenotype as well as NF-κB activation and TGF-β1-induced cell proliferation of endometriotic stromal cells.
    Large scale data: N/A.
    Limitations, reasons for caution: In vivo studies are required to confirm the present in vitro results. However, it remains challenging to mimic non-resolving chronic inflammation in animal models, as active inflammation can resolve spontaneously.
    Wider implications of the findings: Dysfunction of negative regulators of IL-6/sIL-6R/STAT3 signaling may cause persistent activation of STAT3 in endometriosis. Since STAT3 activation in the endometrium is essential for successful embryo implantation, treatment with STAT3 inhibitors would not be appropriate for women wishing to conceive. However, targeting impaired negative regulation of IL-6/sIL-6R/STAT3 signaling may still represent a promising avenue for the treatment of endometriosis.
    Study funding/competing interest(s): This study was supported in part by the KARL STORZ SE & Co. KG (Tuttlingen, Germany). There are no conflicts of interest.
    MeSH term(s) Animals ; Endometriosis/pathology ; Endometrium/metabolism ; Female ; Fibrosis ; Humans ; Inflammation/metabolism ; Interleukin-6/metabolism ; NF-kappa B ; Receptors, Interleukin-6/metabolism ; Receptors, Interleukin-6/therapeutic use ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; STAT3 Transcription Factor/therapeutic use ; Stromal Cells/metabolism
    Chemical Substances Interleukin-6 ; NF-kappa B ; Receptors, Interleukin-6 ; STAT3 Transcription Factor
    Language English
    Publishing date 2022-05-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632776-x
    ISSN 1460-2350 ; 0268-1161 ; 1477-741X
    ISSN (online) 1460-2350
    ISSN 0268-1161 ; 1477-741X
    DOI 10.1093/humrep/deac098
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  5. Article ; Online: Hyperactivation of dormant primordial follicles in ovarian endometrioma patients.

    Matsuzaki, Sachiko / Pankhurst, Michael W

    Reproduction (Cambridge, England)

    2020  Volume 160, Issue 6, Page(s) R145–R153

    Abstract: Serum anti-Müllerian hormone (AMH) levels decrease after surgical treatment of ovarian endometrioma. This is the main reason that surgery for ovarian endometrioma endometriosis is not recommended before in vitro fertilization, unless the patient has ... ...

    Abstract Serum anti-Müllerian hormone (AMH) levels decrease after surgical treatment of ovarian endometrioma. This is the main reason that surgery for ovarian endometrioma endometriosis is not recommended before in vitro fertilization, unless the patient has severe pain or suspected malignant cysts. Furthermore, it has been suggested that ovarian endometrioma itself damages ovarian reserve. This raises two important challenges: (1) determining how to prevent surgical damage to the ovarian reserve in women with ovarian endometrioma and severe pain requiring surgical treatment and (2) deciding the best treatment for women with ovarian endometrioma without pain, who do not wish to conceive immediately. The mechanisms underlying the decline in ovarian reserve are potentially induced by both ovarian endometrioma and surgical injury but the relative contribution of each process has not been determined. Data obtained from various animal models and human studies suggest that hyperactivation of dormant primordial follicles caused by the local microenvironment of ovarian endometrioma (mechanical and/or chemical cues) is the main factor responsible for the decreased primordial follicle numbers in women with ovarian endometrioma. However, surgical injury also induces hyperactivation of dormant primordial follicles, which may further reduce ovarian reserve after removal of the endometriosis. Although further studies are required to elucidate the mechanisms underlying diminished ovarian reserve in women with ovarian endometrioma, the available data strongly suggests the need to prevent/minimize hyperactivation of dormant primordial follicles, regardless of whether surgery is performed, for better clinical management of ovarian endometrioma.
    MeSH term(s) Endometriosis/complications ; Endometriosis/pathology ; Female ; Humans ; Infertility, Female/etiology ; Infertility, Female/pathology ; Ovarian Follicle/pathology ; Ovarian Reserve ; Ovary/pathology
    Language English
    Publishing date 2020-10-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2034501-X
    ISSN 1741-7899 ; 1470-1626 ; 1476-3990
    ISSN (online) 1741-7899
    ISSN 1470-1626 ; 1476-3990
    DOI 10.1530/REP-20-0265
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  6. Article ; Online: Dose-dependent pro- or anti-fibrotic responses of endometriotic stromal cells to interleukin-1β and tumor necrosis factor α.

    Matsuzaki, Sachiko / Pouly, Jean-Luc / Canis, Michel

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 9467

    Abstract: Endometriosis are characterized by dense fibrous tissue. Numerous studies have investigated roles of inflammation on the pathophysiology of endometriosis. However, the interplay of inflammation and fibrosis remains to be clarified. Here we show that low ... ...

    Abstract Endometriosis are characterized by dense fibrous tissue. Numerous studies have investigated roles of inflammation on the pathophysiology of endometriosis. However, the interplay of inflammation and fibrosis remains to be clarified. Here we show that low levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNFα) promoted a fibrotic phenotype, whereas high levels of IL-1β and TNFα inactivated the fibrotic phenotype of endometriotic stromal cells (Ectopic-ES). IL-1β 10 pg/mL and TNFα 100 and 1,000 pg/mL had minimal effects, whereas the highest dose of IL-1β (100 pg/mL) significantly decreased collagen gel contraction in Ectopic-ES. Furthermore, in Ectopic-ES, low levels of IL-1β (1 pg/mL) and/or TNFα 10 pg/mL significantly increased Col I mRNA expression, whereas higher doses of IL-1β (10 and/or 100 pg/mL) and/or TNFα (100 and/or 1,000 pg/mL) significantly decreased Col I and/or αSMA mRNA expression and the percentage of cells with Col I + and/or αSMA + stress fibers. In contrast, in either menstrual endometrial stromal cells of patients with endometriosis or those of healthy women, varying doses of IL-1β and/or TNFα had no significant effects on either Col I or αSMA mRNA/protein expression. The present findings bring into question whether we should still continue to attempt anti-inflammatory treatment strategies for endometriosis.
    MeSH term(s) Adult ; Cells, Cultured ; Endometriosis/metabolism ; Endometrium/metabolism ; Female ; Fibrosis/metabolism ; Humans ; Interleukin-1beta/metabolism ; RNA, Messenger/metabolism ; Stromal Cells/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Young Adult
    Chemical Substances IL1B protein, human ; Interleukin-1beta ; RNA, Messenger ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2020-06-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-66298-x
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  7. Article ; Online: DNA microarray analysis in endometriosis for development of more effective targeted therapies.

    Matsuzaki, Sachiko

    Frontiers in bioscience (Elite edition)

    2011  Volume 3, Issue 3, Page(s) 1139–1153

    Abstract: Microarray technology has become a widely used tool for analyzing the expression of tens of thousands of genes simultaneously on high-density microarrays in a single experiment, together with the availability of the complete nucleotide sequence of the ... ...

    Abstract Microarray technology has become a widely used tool for analyzing the expression of tens of thousands of genes simultaneously on high-density microarrays in a single experiment, together with the availability of the complete nucleotide sequence of the human genome. DNA microarray technologies are powerful tools in the laboratory setting for scientific research, hypothesis generation, and the production of leads for subsequent validation through more sophisticated technologies. Since 2002, and particularly in the past few years, the utility of various DNA microarray technologies in endometriosis has rapidly and tremendously evolved; DNA microarray studies provide extremely important information that enable a better understanding of pathophysiology and disease etiology. This is a review of the literature focused on new findings of endometriosis pathophysiology obtained using various microarray technologies: gene expression profiling, microarray-based comparative genomic hybridization (CGH) (array CGH) single nucleotide polymorphism (SNP) arrays, the combination of chromatin immunoprecipitation (ChIP) with hybridization of microarrays (ChIP-on-chip). The present review discusses the results of a decade of DNA microarray technology experience, with emphasis on the pathophysiology of endometriosis in the context of clinical studies.
    MeSH term(s) Chromatin Immunoprecipitation ; Comparative Genomic Hybridization ; Endometriosis/genetics ; Endometriosis/therapy ; Female ; Gene Expression ; Humans ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide
    Language English
    Publishing date 2011-06-01
    Publishing country Singapore
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2565080-4
    ISSN 1945-0508 ; 1945-0494
    ISSN (online) 1945-0508
    ISSN 1945-0494
    DOI 10.2741/e317
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  8. Article ; Online: Impaired pathogen-induced autophagy and increased IL-1β and TNFα release in response to pathogenic triggers in secretory phase endometrial stromal cells of endometriosis patients.

    Matsuzaki, Sachiko / Gremeau, Anne-Sophie / Pouly, Jean-Luc

    Reproductive biomedicine online

    2020  Volume 41, Issue 5, Page(s) 767–781

    Abstract: Research question: It is not clear whether innate immunity along with autophagy is altered in endometrial cells of patients with endometriosis.: Design: This study evaluated the effects of lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid ( ... ...

    Abstract Research question: It is not clear whether innate immunity along with autophagy is altered in endometrial cells of patients with endometriosis.
    Design: This study evaluated the effects of lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C) stimulation on autophagy induction, pro-IL-1β expression, and secretion of interleukin-1β (IL-1β) and tumour necrosis factor-α (TNFα) in endometrial epithelial and/or stromal cells of patients with endometriosis (EE-endo, ES-endo, respectively), those of patients with hydrosalpinx (EE-hydro, ES-hydro, respectively) and those of healthy fertile women (EE-healthy, ES-healthy, respectively), with and without inhibition of autophagy by autophagy-related (ATG)13 gene small interfering RNA (siRNA).
    Results: Stimulation with either LPS or poly I:C triggered autophagy in EE/ES-healthy, whereas no significant induction was observed in either EE/ES-endo or EE/ES-hydro. In EE- and/or ES-healthy, IL-1β and/or TNFα secretion after stimulation with LPS or poly I:C was significantly higher in cells with ATG13 knockdown compared with those with siRNA control (P < 0.03), whereas no significant difference was observed in either EE/ES-endo or EE/ES-hydro. In the secretory phase ES-endo without autophagy inhibition, IL-1β and TNFα secretion were significantly higher compared with those of ES-healthy after stimulation with either LPS or poly I:C for 4 h (P < 0.001) and for 24 h (P < 0.01).
    Conclusion: Pathogen-induced autophagy was impaired in EE/ES-endo. Increased IL-1β and TNFα release in response to pathogenic triggers in the secretory phase ES-endo may result in the development of an inflammatory uterine microenvironment detrimental to successful embryo implantation.
    MeSH term(s) Adult ; Autophagy/drug effects ; Autophagy/physiology ; Endometriosis/metabolism ; Endometrium/drug effects ; Endometrium/metabolism ; Female ; Humans ; Interleukin-1beta/metabolism ; Lipopolysaccharides/pharmacology ; Poly I-C/pharmacology ; Stromal Cells/drug effects ; Stromal Cells/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Young Adult
    Chemical Substances Interleukin-1beta ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Poly I-C (O84C90HH2L)
    Language English
    Publishing date 2020-06-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2113823-0
    ISSN 1472-6491 ; 1472-6483
    ISSN (online) 1472-6491
    ISSN 1472-6483
    DOI 10.1016/j.rbmo.2020.06.011
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  9. Article ; Online: In vitro and in vivo effects of MK2206 and chloroquine combination therapy on endometriosis: autophagy may be required for regrowth of endometriosis.

    Matsuzaki, Sachiko / Pouly, Jean-Luc / Canis, Michel

    British journal of pharmacology

    2018  Volume 175, Issue 10, Page(s) 1637–1653

    Abstract: Background and purpose: A high recurrence rate after medical treatment is a major clinical problem for patients with endometriosis. Here, we have evaluated the in vitro effects of combined treatment with MK2206 (an AKT inhibitor) + chloroquine on cell ... ...

    Abstract Background and purpose: A high recurrence rate after medical treatment is a major clinical problem for patients with endometriosis. Here, we have evaluated the in vitro effects of combined treatment with MK2206 (an AKT inhibitor) + chloroquine on cell growth and regrowth of endometriotic stromal cells and the in vivo effects on endometriotic implants in a mouse xenograft model of endometriosis.
    Experimental approach: We evaluated the effects of autophagy inhibition by knockdown of the ATG13, Beclin-1 and ATG12 genes and pharmacological agents (chloroquine, bafilomycin A1 or 3-methyalanine) individually and in combination with MK2206 on cell growth and/or cell regrowth of endometriotic stromal cells in vitro. Furthermore, we evaluated treatment with MK2206 + chloroquine on endometriotic implants in a mouse xenograft model of endometriosis.
    Key results: Combined treatment with MK2206 and chloroquine markedly reduced cell growth and regrowth after discontinuation of treatment in endometriotic stromal cells compared with cells treated with either drug alone. Autophagy inhibition by ATG13, Beclin-1 or ATG12 gene knockdown only affected regrowth of endometriotic stromal cells, but not endometrial stromal cells from the same patients, after a 72 h discontinuation of the combined treatment. Furthermore, combined treatment reduced the size of endometriotic implants, whereas no effects on endometriotic implants treated with either drug alone were observed in a mouse xenograft model of endometriosis.
    Conclusions and implications: The present findings suggest that a novel strategy for treatment of endometriosis may involve decreasing the number of endometriotic cells that can survive treatment and then preventing regrowth by autophagy inhibition.
    MeSH term(s) Adult ; Animals ; Autophagy/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Chloroquine/chemistry ; Chloroquine/pharmacology ; Disease Models, Animal ; Drug Therapy, Combination ; Endometriosis/drug therapy ; Endometriosis/pathology ; Female ; Heterocyclic Compounds, 3-Ring/chemistry ; Heterocyclic Compounds, 3-Ring/pharmacology ; Humans ; Mice ; Young Adult
    Chemical Substances Heterocyclic Compounds, 3-Ring ; MK 2206 ; Chloroquine (886U3H6UFF)
    Language English
    Publishing date 2018-04-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.14170
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  10. Article ; Online: Reply to the letter from Barra et al.

    Matsuzaki, Sachiko / Pouly, Jean-Luc / Canis, Michel

    British journal of pharmacology

    2018  Volume 175, Issue 17, Page(s) 3628–3629

    MeSH term(s) Autophagy ; Chloroquine ; Endometriosis ; Female ; Heterocyclic Compounds, 3-Ring ; Humans
    Chemical Substances Heterocyclic Compounds, 3-Ring ; MK 2206 ; Chloroquine (886U3H6UFF)
    Language English
    Publishing date 2018-07-08
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.14390
    Database MEDical Literature Analysis and Retrieval System OnLINE

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