Co-cultured endometrial stromal cells and peritoneal mesothelial cells for an in vitro model of endometriosis

2012 ◽  
Vol 4 (9) ◽  
pp. 1090 ◽  
Author(s):  
Zhenling Chen ◽  
Yi Dai ◽  
Zhe Dong ◽  
Menghui Li ◽  
Xuan Mu ◽  
...  
Keyword(s):  
Stromal Cells ◽  
In Vitro Model ◽  
Mesothelial Cells ◽  
Endometrial Stromal Cells ◽  
Peritoneal Mesothelial Cells ◽  
Vitro Model

Tumor Necrosis Factor-α and Interleukin-1β Treatment of Endometrial Stromal Cells Does not Promote Their Adhesion to Peritoneal Mesothelial Cells in an in Vitro Model of Early-Stage Endometriosis

2011 ◽  
Vol 3 (2) ◽  
pp. 67-72
Author(s):  
Jean-Christophe Lousse ◽  
Sylvie Defrere ◽  
Sébastien Colette ◽  
Anne Van Langendonckt ◽  
Jacques Donnez
Keyword(s):  
Cell Adhesion ◽  
In Vitro Model ◽  
Early Stage ◽  
Mesothelial Cells ◽  
Endometrial Stromal Cells ◽  
Peritoneal Mesothelial Cells ◽  
Pre Treatment ◽  
Vitro Model ◽  
The Impact

In this study, we developed an original and reproducible quantitative in vitro model of endometrial cell adhesion to peritoneal mesothelial cells in order to better assess the impact of pro-inflammatory cytokines on early-stage endometriosis development. We demonstrated that pre-treatment with TNF-α and IL-1β does not promote endometrial stromal cell adhesion to peritoneal mesothelial cells.

Hormonal regulation of human endometrial stromal cells in culture: an in vitro model for decidualization

1989 ◽  
Vol 52 (5) ◽  
pp. 761-768 ◽  
Author(s):  
Juan C. Irwin ◽  
David Kirk ◽  
Roger J.B. King ◽  
Martin M. Quigley ◽  
Ralph B.L. Gwatkin
Keyword(s):  
Stromal Cells ◽  
Hormonal Regulation ◽  
In Vitro Model ◽  
Endometrial Stromal Cells ◽  
Cells In Culture ◽  
Vitro Model

scholarly journals Endometrial inflammasome activation accompanies menstruation and may have implications for systemic inflammatory events of the menstrual cycle

2020 ◽  
Vol 35 (6) ◽  
pp. 1363-1376
Author(s):  
Aida Azlan ◽  
Lois A Salamonsen ◽  
Jennifer Hutchison ◽  
Jemma Evans
Keyword(s):  
Menstrual Cycle ◽  
Stromal Cells ◽  
Nlrp3 Inflammasome ◽  
In Vitro Model ◽  
Inflammasome Activation ◽  
Menstrual Phase ◽  
Secretory Phase ◽  
Endometrial Stromal Cells ◽  
Vitro Model

Abstract STUDY QUESTION Does NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome activation within decidualized endometrial stromal cells accompany menstruation and is this reflected systemically? SUMMARY ANSWER Components of the NLRP3 inflammasome immunolocalize to decidualized endometrial stromal cells immediately prior to menstruation, and are activated in an in vitro model of menstruation, as evidenced by downstream interleukin (IL)-1beta and IL-18 release, this being reflected systemically in vivo. WHAT IS KNOWN ALREADY Menstruation is a highly inflammatory event associated with activation of NFκB (nuclear factor kappa-light-chain-enhancer of activated B cells), local release of chemokines and cytokines and inflammatory leukocyte influx. Systemically, chemokines and cytokines fluctuate across the menstrual cycle. STUDY DESIGN, SIZE, DURATION This study examined the NLRP3 inflammasome and activation of downstream IL-1beta and IL-18 in endometrial tissues from women of known fertility (≥1 previous parous pregnancy) across the menstrual cycle (n ≥ 8 per cycle phase), serum from women during the proliferative, secretory and menstrual phases (≥9 per cycle phase) of the cycle and menstrual fluid collected on Day 2 of menses (n = 18). Endometrial stromal cells isolated from endometrial tissue biopsies (n = 10 in total) were used for an in vitro model of pre-menstrual hormone withdrawal. PARTICIPANTS/MATERIALS, SETTING, METHODS Expression and localization of components of the NLRP3 inflammasome (NLRP3 & apoptosis-associated speck–caspase recruit domain [ASC]) in endometrial tissues was performed by immunohistochemistry. Unbiased digital quantification of immunohistochemical staining allowed determination of different patterns of expression across the menstrual cycle. Serum from women across the menstrual cycle was examined for IL-1beta and IL-18 concentrations by ELISA. An in vitro model of hormone withdrawal from estrogen/progestin decidualized endometrial stromal cells was used to more carefully examine activation of the NLRP3 inflammasome. Endometrial stromal cells isolated from endometrial tissue biopsies (n = 10) were treated with estrogen/medroxyprogesterone acetate for 12 days to induce decidualization (assessed by release of prolactin) followed by withdrawal of steroid hormone support. Activation of NLRP3, & ASC in these cells was examined on Days 0–3 after hormone withdrawal by Western immunoblotting. Release of IL-1beta and IL-18 examined during decidualization and across the same time course of hormone withdrawal by ELISA. Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal. MAIN RESULTS AND THE ROLE OF CHANCE Critical components of the NLRP3 inflammasome (NLRP3, ASC) were increased in menstrual phase endometrial tissues versus early secretory phase tissues (P < 0.05, n/s, respectively). NLRP3 and ASC were also elevated in the proliferative versus secretory phase of the cycle (P < 0.01, n/s, respectively) with ASC also significantly increased in the late-secretory versus early-secretory phase (P < 0.05). The pattern of activation was reflected in systemic levels of the inflammasome mediators, with IL-1beta and IL-18 elevated in peripheral blood serum during menstruation (Day 2 of menses) versus secretory phase (P = 0.026, P = 0.0042, respectively) and significantly elevated in menstrual fluid (Day 2 of menses) versus systemic levels across all cycle phases, suggesting that local inflammasome activation within the endometrium during menses is reflected by systemic inflammation. NLRP3 and ASC localized to decidualized cells adjacent to the spiral arterioles in the late secretory phase of the menstrual cycle, where the menstrual cascade is thought to be initiated, and to endometrial leukocytes during the menstrual phase. NLRP3 also localized to glandular epithelial cells during the late-secretory/menstrual phases. Localization of both NLRP3 and ASC switched from predominant epithelial localization during the early-secretory phase to stromal localization during the late-secretory/menstrual phase. Using an in vitro model of hormone withdrawal from decidualized human endometrial stromal cells, we demonstrated progressive activation of NLRP3 and ASC after hormone withdrawal increasing from Day 0 of withdrawal/Day 12 of decidualization to Day 3 of withdrawal. Downstream release of IL-1beta and IL-18 from decidualized stromal cells after hormone withdrawal followed the same pattern with the role of NLRP3 inflammasome activation confirmed via the inhibition of IL-1beta and IL-18 release upon application of MCC950. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION This study uses descriptive and semi-quantitative measures of NLRP3 inflammasome activation within endometrial tissues. Further, the in vitro model of pre-menstrual hormone withdrawal may not accurately recapitulate the in vivo environment as only one cell type is present and medroxyprogesterone acetate replaced natural progesterone due to its longer stability. WIDER IMPLICATIONS OF THE FINDINGS We provide novel evidence that the NLRP3 inflammasome is activated within decidualized endometrial stromal cells immediately prior to menses and that local activation of the inflammasome within the endometrium appears to be reflected systemically in by activation of downstream IL-1beta and IL-18. Given the prevalence of menstrual disorders associated with inflammation including dysmenorrhoea and aspects of pre-menstrual syndrome, the inflammasome could be a novel target for ameliorating such burdens. STUDY FUNDING/COMPETING INTEREST(S) The authors have no competing interests. J.E. was supported by a Fielding Foundation fellowship, NHMRC project grants (#1139489 and #1141946) and The Hudson Institute of Medical Research. L.A.S. was supported by The Hudson Institute of Medical Research and J.H. by an Australian Government Research Training Program Scholarship. We acknowledge the Victorian Government’s Operating Infrastructure funding to the Hudson Institute. TRIAL REGISTRATION NUMBER N/A

scholarly journals Extracellular Vesicles Are More Potent Than Adipose Mesenchymal Stromal Cells to Exert an Anti-Fibrotic Effect in an In Vitro Model of Systemic Sclerosis

2021 ◽  
Vol 22 (13) ◽  
pp. 6837
Author(s):  
Pauline Rozier ◽  
Marie Maumus ◽  
Claire Bony ◽  
Alexandre Thibault Jacques Maria ◽  
Florence Sabatier ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Extracellular Vesicles ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
In Vitro Model ◽  
Specific Treatment ◽  
Complex Disorder ◽  
Molecular Features ◽  
Vitro Model

Systemic sclerosis (SSc) is a complex disorder resulting from dysregulated interactions between the three main pathophysiological axes: fibrosis, immune dysfunction, and vasculopathy, with no specific treatment available to date. Adipose tissue-derived mesenchymal stromal cells (ASCs) and their extracellular vesicles (EVs) have proved efficacy in pre-clinical murine models of SSc. However, their precise action mechanism is still not fully understood. Because of the lack of availability of fibroblasts isolated from SSc patients (SSc-Fb), our aim was to determine whether a TGFβ1-induced model of human myofibroblasts (Tβ-Fb) could reproduce the characteristics of SSc-Fb and be used to evaluate the anti-fibrotic function of ASCs and their EVs. We found out that Tβ-Fb displayed the main morphological and molecular features of SSc-Fb, including the enlarged hypertrophic morphology and expression of several markers associated with the myofibroblastic phenotype. Using this model, we showed that ASCs were able to regulate the expression of most myofibroblastic markers on Tβ-Fb and SSc-Fb, but only when pre-stimulated with TGFβ1. Of interest, ASC-derived EVs were more effective than parental cells for improving the myofibroblastic phenotype. In conclusion, we provided evidence that Tβ-Fb are a relevant model to mimic the main characteristics of SSc fibroblasts and investigate the mechanism of action of ASCs. We further reported that ASC-EVs are more effective than parental cells suggesting that the TGFβ1-induced pro-fibrotic environment may alter the function of ASCs.

Mesothelial Cells

2007 ◽  
Vol 27 (2_suppl) ◽  
pp. 110-115 ◽  
Author(s):  
Susan Yung ◽  
Chan Tak Mao
Keyword(s):  
Mesothelial Cell ◽  
In Vitro Models ◽  
Mesothelial Cells ◽  
Dynamic Membrane ◽  
Peritoneal Mesothelial Cells ◽  
Immunohistochemical Markers ◽  
Vitro Model ◽  
And Function

♦ Background The introduction of peritoneal dialysis (PD) as a modality of renal replacement therapy has provoked much interest in the biology of the peritoneal mesothelial cell. Mesothelial cells isolated from omental tissue have immunohistochemical markers that are identical to those of mesothelial stem cells, and omental mesothelial cells can be cultivated in vitro to study changes to their biologic functions in the setting of PD. ♦ Method The present article describes the structure and function of mesothelial cells in the normal peritoneum and details the morphologic changes that occur after the introduction of PD. Furthermore, this article reviews the literature of mesothelial cell culture and the limitations of in vitro studies. ♦ Results The mesothelium is now considered to be a dynamic membrane that plays a pivotal role in the homeostasis of the peritoneal cavity, contributing to the control of fluid and solute transport, inflammation, and wound healing. These functional properties of the mesothelium are compromised in the setting of PD. Cultures of peritoneal mesothelial cells from omental tissue provide a relevant in vitro model that allows researchers to assess specific molecular pathways of disease in a distinct population of cells. Structural and functional attributes of mesothelial cells are discussed in relation to long-term culture, proliferation potential, age of tissue donor, use of human or animal in vitro models, and how the foregoing factors may influence in vitro data. ♦ Conclusions The ability to propagate mesothelial cells in culture has resulted, over the past two decades, in an explosion of mesothelial cell research pertaining to PD and peritoneal disorders. Independent researchers have highlighted the potential use of mesothelial cells as targets for gene therapy or transplantation in the search to provide therapeutic strategies for the preservation of the mesothelium during chemical or bacterial injury.

Exosome derived from murine adipose-derived stromal cells: Neuroprotective effect on in vitro model of amyotrophic lateral sclerosis

2016 ◽  
Vol 340 (1) ◽  
pp. 150-158 ◽  
Author(s):  
Roberta Bonafede ◽  
Ilaria Scambi ◽  
Daniele Peroni ◽  
Valentina Potrich ◽  
Federico Boschi ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Stromal Cells ◽  
In Vitro Model ◽  
Neuroprotective Effect ◽  
Adipose Derived Stromal Cells ◽  
Vitro Model ◽  
Lateral Sclerosis

Growth factor and cytokine expression of human mesenchymal stromal cells is not altered in an in vitro model of tissue damage

Cytotherapy ◽  
2010 ◽  
Vol 12 (7) ◽  
pp. 870-880 ◽  
Author(s):  
Katrin Montzka ◽  
Tobias Führmann ◽  
Jochen Müller-Ehmsen ◽  
Michael Wöltje ◽  
Gary A. Brook
Keyword(s):  
Growth Factor ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Tissue Damage ◽  
In Vitro Model ◽  
Cytokine Expression ◽  
Human Mesenchymal Stromal Cells ◽  
Vitro Model
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