Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis

Objective To quantitate antiapoptotic and proapoptotic gene expression in endometrial cells (ECs) of women with and without endometriosis. Design Determination of transcript abundance (TA) of apoptosis-regulating genes in eutopic and ectopic endometrial cells. Setting Institute for the Study and Tre...

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Veröffentlicht in:Fertility and sterility 2007-02, Vol.87 (2), p.263-268
Hauptverfasser: Braun, Donald P., Ph.D, Ding, Jianchi, Ph.D, Shaheen, Fehr, M.D, Willey, James C., M.D, Rana, Nasir, M.D, Dmowski, W. Paul, M.D., Ph.D
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container_end_page 268
container_issue 2
container_start_page 263
container_title Fertility and sterility
container_volume 87
creator Braun, Donald P., Ph.D
Ding, Jianchi, Ph.D
Shaheen, Fehr, M.D
Willey, James C., M.D
Rana, Nasir, M.D
Dmowski, W. Paul, M.D., Ph.D
description Objective To quantitate antiapoptotic and proapoptotic gene expression in endometrial cells (ECs) of women with and without endometriosis. Design Determination of transcript abundance (TA) of apoptosis-regulating genes in eutopic and ectopic endometrial cells. Setting Institute for the Study and Treatment of Endometriosis, Chicago, Illinois, and university-based research laboratories. Patient(s) Women with (n = 10) and without (n = 6) endometriosis. Intervention(s) None. Main Outcome Measure(s) Quantitative virtually multiplexed transcript abundance measurement (VMTA) of the BCL2, BCLxL, defender against cell death-1 (DAD-1), BCLxS, P53, Caspase-1, and proliferating cell nuclear antigen (PCNA) genes. Result(s) The TA ratio of antiapoptotic to proapoptotic isoforms of the BCL-X gene favors survival in eutopic and ectopic ECs from women with endometriosis, but not control ECs. This was found throughout the menstrual cycle for ectopic ECs. Eutopic but not ectopic ECs also expressed increased TA of the antiapoptotic DAD-1 gene in endometriosis. Eutopic and ectopic ECs from women with endometriosis expressed decreased TA of p53 and Caspase-1 compared to ECs from women without endometriosis. Expression of these genes was not correlated with the proliferative state of ECs based on TA of the PCNA gene. Conclusion(s) Dysregulation in expression of pro- and antiapoptotic regulatory genes characterizes eutopic and ectopic ECs from women with endometriosis. These results are consistent with apoptotic resistance and enhanced survival of ECs in endometriosis.
doi_str_mv 10.1016/j.fertnstert.2006.06.026
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Result(s) The TA ratio of antiapoptotic to proapoptotic isoforms of the BCL-X gene favors survival in eutopic and ectopic ECs from women with endometriosis, but not control ECs. This was found throughout the menstrual cycle for ectopic ECs. Eutopic but not ectopic ECs also expressed increased TA of the antiapoptotic DAD-1 gene in endometriosis. Eutopic and ectopic ECs from women with endometriosis expressed decreased TA of p53 and Caspase-1 compared to ECs from women without endometriosis. Expression of these genes was not correlated with the proliferative state of ECs based on TA of the PCNA gene. Conclusion(s) Dysregulation in expression of pro- and antiapoptotic regulatory genes characterizes eutopic and ectopic ECs from women with endometriosis. 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Paul, M.D., Ph.D</creatorcontrib><title>Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis</title><title>Fertility and sterility</title><addtitle>Fertil Steril</addtitle><description>Objective To quantitate antiapoptotic and proapoptotic gene expression in endometrial cells (ECs) of women with and without endometriosis. Design Determination of transcript abundance (TA) of apoptosis-regulating genes in eutopic and ectopic endometrial cells. Setting Institute for the Study and Treatment of Endometriosis, Chicago, Illinois, and university-based research laboratories. Patient(s) Women with (n = 10) and without (n = 6) endometriosis. Intervention(s) None. Main Outcome Measure(s) Quantitative virtually multiplexed transcript abundance measurement (VMTA) of the BCL2, BCLxL, defender against cell death-1 (DAD-1), BCLxS, P53, Caspase-1, and proliferating cell nuclear antigen (PCNA) genes. Result(s) The TA ratio of antiapoptotic to proapoptotic isoforms of the BCL-X gene favors survival in eutopic and ectopic ECs from women with endometriosis, but not control ECs. This was found throughout the menstrual cycle for ectopic ECs. Eutopic but not ectopic ECs also expressed increased TA of the antiapoptotic DAD-1 gene in endometriosis. Eutopic and ectopic ECs from women with endometriosis expressed decreased TA of p53 and Caspase-1 compared to ECs from women without endometriosis. Expression of these genes was not correlated with the proliferative state of ECs based on TA of the PCNA gene. Conclusion(s) Dysregulation in expression of pro- and antiapoptotic regulatory genes characterizes eutopic and ectopic ECs from women with endometriosis. These results are consistent with apoptotic resistance and enhanced survival of ECs in endometriosis.</description><subject>Adult</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - analysis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>endometriosis</subject><subject>Endometriosis - metabolism</subject><subject>endometrium</subject><subject>Endometrium - metabolism</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gene Expression Profiling</subject><subject>Gynecology. Andrology. 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Paul, M.D., Ph.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis</atitle><jtitle>Fertility and sterility</jtitle><addtitle>Fertil Steril</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>87</volume><issue>2</issue><spage>263</spage><epage>268</epage><pages>263-268</pages><issn>0015-0282</issn><eissn>1556-5653</eissn><coden>FESTAS</coden><abstract>Objective To quantitate antiapoptotic and proapoptotic gene expression in endometrial cells (ECs) of women with and without endometriosis. Design Determination of transcript abundance (TA) of apoptosis-regulating genes in eutopic and ectopic endometrial cells. Setting Institute for the Study and Treatment of Endometriosis, Chicago, Illinois, and university-based research laboratories. Patient(s) Women with (n = 10) and without (n = 6) endometriosis. Intervention(s) None. Main Outcome Measure(s) Quantitative virtually multiplexed transcript abundance measurement (VMTA) of the BCL2, BCLxL, defender against cell death-1 (DAD-1), BCLxS, P53, Caspase-1, and proliferating cell nuclear antigen (PCNA) genes. Result(s) The TA ratio of antiapoptotic to proapoptotic isoforms of the BCL-X gene favors survival in eutopic and ectopic ECs from women with endometriosis, but not control ECs. This was found throughout the menstrual cycle for ectopic ECs. Eutopic but not ectopic ECs also expressed increased TA of the antiapoptotic DAD-1 gene in endometriosis. Eutopic and ectopic ECs from women with endometriosis expressed decreased TA of p53 and Caspase-1 compared to ECs from women without endometriosis. Expression of these genes was not correlated with the proliferative state of ECs based on TA of the PCNA gene. Conclusion(s) Dysregulation in expression of pro- and antiapoptotic regulatory genes characterizes eutopic and ectopic ECs from women with endometriosis. 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source MEDLINE; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection
subjects Adult
Apoptosis
Apoptosis Regulatory Proteins - analysis
Biological and medical sciences
Biomarkers - analysis
endometriosis
Endometriosis - metabolism
endometrium
Endometrium - metabolism
Female
Female genital diseases
Gene Expression Profiling
Gynecology. Andrology. Obstetrics
Humans
Internal Medicine
Medical sciences
mRNA
Non tumoral diseases
Obstetrics and Gynecology
title Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis
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