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2. Endometrial stromal fibroblasts from women with polycystic ovary syndrome have impaired progesterone-mediated decidualization, aberrant cytokine profiles and promote enhanced immune cell migration in vitro

Author

Piltonen, TT, Chen, JC, Khatun, M, Kangasniemi, M, Liakka, A, Spitzer, T, Tran, N, Huddleston, H, Irwin, JC, and Giudice, LC

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Contraception/Reproduction, Clinical Research, Infertility, 2.1 Biological and endogenous factors, Aetiology, Reproductive health and childbirth, Adult, Biopsy, Case-Control Studies, Cell Movement, Cell Proliferation, Cytokines, Decidua, Embryo Implantation, Endometrial Neoplasms, Endometrium, Estrogens, Female, Fibroblasts, Gene Expression Regulation, Genetic Predisposition to Disease, Glucose Tolerance Test, Humans, Middle Aged, Polycystic Ovary Syndrome, Pregnancy, Progesterone, Prospective Studies, PCOS, endometrium, decidualization, cytokines, MMP, Medical and Health Sciences, Studies in Human Society, Obstetrics & Reproductive Medicine, Reproductive medicine
Abstract

Study questionDo endometrial stromal fibroblasts (eSF) in women with polycystic ovary syndrome (PCOS) (eSFpcos) exhibit altered estrogen and/or progesterone (P4) responses, which may explain some of the adverse reproductive outcomes and endometrial pathologies in these women?Summary answerIn vitro, eSF from women with PCOS exhibit an aberrant decidualization response and concomitant changes in pro-inflammatory cytokine, chemokine and matrix metalloproteinase (MMP) release and immune cell chemoattraction. In vivo these aberrations may result in suboptimal implantation and predisposition to endometrial cancer.What is known alreadyThe endometrium in women with PCOS has several abnormalities including progesterone (P4) resistance at the gene expression level, likely contributing to subfertility, pregnancy complications and increased endometrial cancer risk in PCOS women.Study design, size, durationProspective, university-based, case-control, in vitro study.Participants/materials, setting, methodsCultures of eSFPCOS (n = 12, Rotterdam and NIH criteria) and eSFControl (Ctrl) (n = 6, regular cycle length, no signs of hyperandrogenism) were treated with vehicle, estradiol (E2, 10 nM) or E2P4 (10 nM/1 μM) for 14 days. Progesterone receptor (PGR) mRNA was assessed with quantitative real-time PCR (qRT-PCR) and eSF decidualization was confirmed by insulin-like growth factor-binding protein-1 (IGFBP-1) transcript and protein expression. Fractalkine (CX3CL1), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL) 6, 8 and 11, macrophage chemoattractant protein (MCP) 1 and 3, CCL5 (RANTES) and MMPs (MMP1, 2, 3, 7, 9, 10 and 12) were measured in conditioned media by Luminex multiplex assays, and chemotactic activity of the conditioned media was tested in a migration assay using CD14+ monocyte and CD4+ T-cell migration assay. Effects of IL-6 (0.02, 0.2, 2 or 20 ng/ml) or IL-8 (0.04, 0.4, 4, or 40 ng/ml) or combination (0.2 ng/ml IL-6 and 4.0 ng/ml IL-8) on 14-d decidualization were also tested. ANOVA with pre-planned contrasts was used for statistical analysis.Main results and the role of chanceHormonal challenge with E2P4 to induce decidualization revealed two distinct subsets of eSFPCOS. Eight eSFPCOS (dPCOS) and all eSFCtrl (dCtrl) cultures showed a normal decidualization response to E2P4 as determined by morphology and IGFBP-1 secretion. However, 4 eSFPCOS cultures showed blunted decidualization (ndPCOS) in morphological assessment and low IGFBP-1 levels even though all three groups exhibited normal estrogen-mediated increase in PGR expression. Interestingly dPCOS had decreased IL-6 and GM-SCF secretion compared with dCtrl, whereas the ndPCOS cultures showed increased IL-6 and 8, MCP1, RANTES and GM-CSF secretion at base-line and/or in response to E2 or E2P4 compared with dCtrl and/or dPCOS. Furthermore, even though PGR expression was similar in all three groups, P4 inhibition of MMP secretion was attenuated in ndPCOS resulting in higher MMP2 and 3 levels. The conditioned media from ndPCOS had increased chemoattractic activity compared with dCtrl and dPCOS media. Exogenously added IL-6 and/or 8 did not inhibit decidualization in eSFCtrl indicating that high levels of these cytokines in ndPCOS samples were not likely a cause for the aberrant decidualization.Limitations, reasons for cautionThis is an in vitro study with a small sample size, utilizing stromal cell cultures from proliferative and secretory phase endometrium. The effect of PCOS on endometrial epithelium, another major histoarchitectural cell compartment of the endometrium, was not evaluated and should be considered in future studies. Furthermore, results obtained should also be confirmed in a larger data set and with mid/late secretory phase in vivo samples and models.Wider implications of the findingsThe alterations seen in ndPCOS may contribute to endometrial dysfunction, subfertility and pregnancy complications in PCOS women. The results emphasize the importance of understanding immune responses related to the implantation process and normal endometrial homeostasis in women with PCOS.Study funding/competing interestsSigrid Juselius Foundation, Academy of Finland, Finnish Medical Foundation, Orion-Farmos Research Foundation (to T.T.P.), the NIH Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) U54HD 055764-07 Specialized Cooperative Centers Program in Reproduction and Infertility Research (to L.C.G.), the NICHD the Ruth L. Kirschstein National Research Service Awards grant 1F32HD074423-03 (to J.C.C.). The authors have no competing interests.

Published
2015

8. GvHD after umbilical cord blood transplantation for acute leukemia: an analysis of risk factors and effect on outcomes

Author

Chen, Y-B, Wang, T, Hemmer, M T, Brady, C, Couriel, D R, Alousi, A, Pidala, J, Urbano-Ispizua, A, Choi, S W, Nishihori, T, Teshima, T, Inamoto, Y, Wirk, B, Marks, D I, Abdel-Azim, H, Lehmann, L, Yu, L, Bitan, M, Cairo, M S, Qayed, M, Salit, R, Gale, R P, Martino, R, Jaglowski, S, Bajel, A, Savani, B, Frangoul, H, Lewis, I D, Storek, J, Askar, M, Kharfan-Dabaja, M A, Aljurf, M, Ringden, O, Reshef, R, Olsson, R F, Hashmi, S, Seo, S, Spitzer, T R, MacMillan, M L, Lazaryan, A, Spellman, S R, Arora, M, and Cutler, C S

Published
2017
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41. People-wise organizations: the human side of change

Author

Spitzer, T. Quinn and Tobia, Peter M.

Subjects
Human resource management -- Models, Corporate reorganizations -- Models, Business, general, Models
Abstract

You can try all you want to initiate change with elaborate charts and graphs. But you won't get anywhere until you include people in the mix. Discussions about change are [...]

Published
1994

42. Thinking and managing beyond the boundaries

Author

Spitzer, T. Quinn and Tregoe, Benjamin

Subjects
Management -- Methods, International business enterprises -- Management -- Methods, Business, general, Business, Company business management, Management, Methods
Abstract

Two decades ago, Peter Drucker wrote an article entitled, 'What We Can Learn from the Japanese.' The article drew modest attention from a business world that viewed Japan as an [...]

Published
1993

44. Lessons to bring home from wars and recessions

Author

Spitzer, T. Quinn and Tobia, Peter M.

Subjects
Persian Gulf War, 1991 -- Influence -- Economic aspects -- Management, Strategic planning (Business) -- Management -- Economic aspects, Management -- Economic aspects, Recessions -- Management -- Economic aspects, Business, general, Company business management, Influence, Management, Economic aspects
Abstract

Lessons to Bring Home From Wars and Recessions Operation Desert Storm hasn't been the only battle fought by the United States recently. The current recession has been waging war on [...]

Published
1991

48. Try managing costs, not cutting them

Author

Spitzer, T. Quinn and Tobia, Peter M.

Subjects
Cost control -- Methods, Corporations -- Finance, Cost (Economics) -- Methods, General interest, News, opinion and commentary, Company financing, Cost reduction, Finance, Methods
Abstract

MAKE NO MISTAKE about it, the 1990s are the cost-cutting decade. Downsizing, restructuring, re-engineering --whatever the politically correct circumlocution--this is a time of corporate meltdown. Americans have come a long [...]

Published
1993

49. Human endometrial fibroblasts derived from mesenchymal progenitors inherit progesterone resistance and acquire an inflammatory phenotype in the endometrial niche in endometriosis

Author

Barragan, F. (Fatima), Irwin, J. C. (Juan C.), Balayan, S. (Shaina), Erikson, D. W. (David W.), Chen, J. C. (Joseph C.), Houshdaran, S. (Sahar), Piltonen, T. T. (Terhi T.), Spitzer, T. L. (Trimble L.B.), George, A. (Ashley), Rabban, J. T. (Joseph T.), Nezhat, C. (Camran), Giudice, L. C. (Linda C.), Barragan, F. (Fatima), Irwin, J. C. (Juan C.), Balayan, S. (Shaina), Erikson, D. W. (David W.), Chen, J. C. (Joseph C.), Houshdaran, S. (Sahar), Piltonen, T. T. (Terhi T.), Spitzer, T. L. (Trimble L.B.), George, A. (Ashley), Rabban, J. T. (Joseph T.), Nezhat, C. (Camran), and Giudice, L. C. (Linda C.)

Abstract

Human endometrium undergoes cyclic regeneration involving stem/progenitor cells, but the role of resident endometrial mesenchymal stem cells (eMSC) as progenitors of endometrial stromal fibroblasts (eSF) has not been definitively demonstrated. In endometriosis, eSF display progesterone (P₄) resistance with impaired decidualization in vivo and in vitro. To investigate eMSC as precursors of eSF and whether endometriosis P₄ resistance is inherited from eMSC, we analyzed transcriptomes of eutopic endometrium eMSC and eSF isolated by fluorescence-activated cell sorting (FACS) from endometriosis (eMSCendo, eSFendo) and controls (eMSCcontrol, eSFcontrol) and their derived primary cultures. Differentially expressed lineage-associated genes (LG) of FACS-isolated eMSC and eSF were largely conserved in endometriosis. In culture, eSFcontrol maintained in vitro expression of a subset of eSF LG and decidualized in vitro with P₄. The eMSCcontrol cultures differentiated in vitro to eSF lineage, down-regulating eMSC LG and up-regulating eSF LG, showing minimal transcriptome differences versus eSFcontrol cultures and decidualizing in vitro. Cultured eSFendo displayed less in vitro LG stability and did not decidualize in vitro. In vitro, eMSCendo differentiated to eSF lineage but showed more differentially expressed genes versus eSFendo cultures, and did not decidualize in vitro, demonstrating P₄ resistance inherited from eMSCendo. Compared to controls, cultures from tissue-derived eSFendo uniquely had a pro-inflammatory phenotype not present in eMSCendo differentiated to eSF in vitro, suggesting divergent niche effects for in vivo versus in vitro lineage differentiation. These findings substantiate eMSC as progenitors of eSF and reveal eSF in endometriosis as having P₄ resistance inherited from eMSC and a pro-inflammatory phenotype acquired within the endometrial niche.

Published
2016

50. GvHD after umbilical cord blood transplantation for acute leukemia: an analysis of risk factors and effect on outcomes

Author

Chen, Y-B, primary, Wang, T, additional, Hemmer, M T, additional, Brady, C, additional, Couriel, D R, additional, Alousi, A, additional, Pidala, J, additional, Urbano-Ispizua, A, additional, Choi, S W, additional, Nishihori, T, additional, Teshima, T, additional, Inamoto, Y, additional, Wirk, B, additional, Marks, D I, additional, Abdel-Azim, H, additional, Lehmann, L, additional, Yu, L, additional, Bitan, M, additional, Cairo, M S, additional, Qayed, M, additional, Salit, R, additional, Gale, R P, additional, Martino, R, additional, Jaglowski, S, additional, Bajel, A, additional, Savani, B, additional, Frangoul, H, additional, Lewis, I D, additional, Storek, J, additional, Askar, M, additional, Kharfan-Dabaja, M A, additional, Aljurf, M, additional, Ringden, O, additional, Reshef, R, additional, Olsson, R F, additional, Hashmi, S, additional, Seo, S, additional, Spitzer, T R, additional, MacMillan, M L, additional, Lazaryan, A, additional, Spellman, S R, additional, Arora, M, additional, and Cutler, C S, additional

Published
2016
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