{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/44752"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/44752","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Role of transcription factor Runx1 in uterine stromal cell differentiation and maternal-fetal interaction during mouse pregnancy","abstract":"The differentiation of endometrial stromal cells to decidual cells, a process known as decidualization, is essential for the establishment of pregnancy. The decidual tissue produces multitude of factors that control a variety of physiological processes at the fetal-maternal interface, such as endometrial vasculogenesis, modulation of maternal immune response, spiral artery modification and trophoblast invasion. An aberrant decidual response is associated with various pregnancy disorders, including spontaneous miscarriage, intrauterine growth restriction and preeclampsia. Our study revealed that the expression of Runx1, a transcription factor belonging to the runt-domain family, is markedly elevated in the uterine stromal cells during decidualization. Conditional deletion of the uterine Runx1 gene led to severe embryo growth retardation and pregnancy loss during mid-gestation. Histological analysis of the Runx1-null uteri at gestation days 10-12 revealed an abnormally dense decidual tissue resulting from enhanced proliferation, impaired differentiation, and lack of apoptosis of stromal cells. The loss of Runx1 expression in uterine stromal cells also resulted in a marked impairment in the development of maternal blood vessels concomitant with a marked down regulation of several angiogenic factors, such as VEGF-A and angiopoietin-2. Furthermore, immunohistochemical analysis of smooth muscle actin and cytokeratin in the uterine sections of the mutant mice revealed a lack of maternal spiral artery modification and restricted trophoblast invasion. Collectively, these studies demonstrated that in the absence of Runx1 the decidua fails to produce critical factors that impact blood vessel formation, spiral artery modification, stromal apoptosis, and trophoblast migration. Thus, the Runx1-conditional knockout mouse presents an important animal model to study the molecular pathways that operate at the maternal-fetal interphase to control events that are critical for maintenance of pregnancy.","abstract_html":"The differentiation of endometrial stromal cells to decidual cells, a process known as decidualization, is essential for the establishment of pregnancy. The decidual tissue produces multitude of factors that control a variety of physiological processes at the fetal-maternal interface, such as endometrial vasculogenesis, modulation of maternal immune response, spiral artery modification and trophoblast invasion. An aberrant decidual response is associated with various pregnancy disorders, including spontaneous miscarriage, intrauterine growth restriction and preeclampsia. Our study revealed that the expression of Runx1, a transcription factor belonging to the runt-domain family, is markedly elevated in the uterine stromal cells during decidualization. Conditional deletion of the uterine Runx1 gene led to severe embryo growth retardation and pregnancy loss during mid-gestation. Histological analysis of the Runx1-null uteri at gestation days 10-12 revealed an abnormally dense decidual tissue resulting from enhanced proliferation, impaired differentiation, and lack of apoptosis of stromal cells. The loss of Runx1 expression in uterine stromal cells also resulted in a marked impairment in the development of maternal blood vessels concomitant with a marked down regulation of several angiogenic factors, such as VEGF-A and angiopoietin-2. Furthermore, immunohistochemical analysis of smooth muscle actin and cytokeratin in the uterine sections of the mutant mice revealed a lack of maternal spiral artery modification and restricted trophoblast invasion. Collectively, these studies demonstrated that in the absence of Runx1 the decidua fails to produce critical factors that impact blood vessel formation, spiral artery modification, stromal apoptosis, and trophoblast migration. Thus, the Runx1-conditional knockout mouse presents an important animal model to study the molecular pathways that operate at the maternal-fetal interphase to control events that are critical for maintenance of pregnancy.","abstract_has_math":false,"creators":["Athilakshmi, Kannan"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"M.S.","degree_level":"Thesis","degree_discipline":"VMS - Comparative Biosciences","degree_department":null,"school":null,"contributors":["Bagchi, Indrani C."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-05-28T19:18:17Z","date_published":"2013-05-28T19:18:17Z","updated_at":"2026-07-22T22:25:34Z","subjects":["Decidualization","differentiation","Proliferation","Angiogenesis","spiral artery modification","trophoblast migration","maternal-fetal interaction."],"languages":["en"],"rights":["Copyright 2013 Kannan Athilakshmi"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2142/44752","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Bagchi, Indrani C."]},{"key":"dc:creator","label":"Author","values":["Athilakshmi, Kannan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2013-05-28T19:18:17Z","2015-05-28T10:01:46Z","2013-05"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["VMS - Comparative Biosciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M.S."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Decidualization","differentiation","Proliferation","Angiogenesis","spiral artery modification","trophoblast migration","maternal-fetal interaction."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2013 Kannan Athilakshmi"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/44752"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The differentiation of endometrial stromal cells to decidual cells, a process known as decidualization, is essential for the establishment of pregnancy. The decidual tissue produces multitude of factors that control a variety of physiological processes at the fetal-maternal interface, such as endometrial vasculogenesis, modulation of maternal immune response, spiral artery modification and trophoblast invasion. An aberrant decidual response is associated with various pregnancy disorders, including spontaneous miscarriage, intrauterine growth restriction and preeclampsia. Our study revealed that the expression of Runx1, a transcription factor belonging to the runt-domain family, is markedly elevated in the uterine stromal cells during decidualization. Conditional deletion of the uterine Runx1 gene led to severe embryo growth retardation and pregnancy loss during mid-gestation. Histological analysis of the Runx1-null uteri at gestation days 10-12 revealed an abnormally dense decidual tissue resulting from enhanced proliferation, impaired differentiation, and lack of apoptosis of stromal cells. The loss of Runx1 expression in uterine stromal cells also resulted in a marked impairment in the development of maternal blood vessels concomitant with a marked down regulation of several angiogenic factors, such as VEGF-A and angiopoietin-2. Furthermore, immunohistochemical analysis of smooth muscle actin and cytokeratin in the uterine sections of the mutant mice revealed a lack of maternal spiral artery modification and restricted trophoblast invasion. Collectively, these studies demonstrated that in the absence of Runx1 the decidua fails to produce critical factors that impact blood vessel formation, spiral artery modification, stromal apoptosis, and trophoblast migration. Thus, the Runx1-conditional knockout mouse presents an important animal model to study the molecular pathways that operate at the maternal-fetal interphase to control events that are critical for maintenance of pregnancy.","Item withdrawn by Mark Zulauf (zulauf@illinois.edu) on 2013-03-28T19:10:13Z Item was in collections: University of Illinois Theses & Dissertations (ID: 1) No. of bitstreams: 2 Athilakshmi_Kannan thesis final.docx: 81662150 bytes, checksum: dc8acc270ed1c6fcc257f17044eb2411 (MD5) Athilakshmi_Kannan.pdf: 3943258 bytes, checksum: db21a0dfd85da8c1be7d0d199faa55f9 (MD5)","Made available in DSpace on 2013-05-28T19:18:17Z (GMT). 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The decidual tissue produces multitude of factors that control a variety of physiological processes at the fetal-maternal interface, such as endometrial vasculogenesis, modulation of maternal immune response, spiral artery modification and trophoblast invasion. An aberrant decidual response is associated with various pregnancy disorders, including spontaneous miscarriage, intrauterine growth restriction and preeclampsia. Our study revealed that the expression of Runx1, a transcription factor belonging to the runt-domain family, is markedly elevated in the uterine stromal cells during decidualization. Conditional deletion of the uterine Runx1 gene led to severe embryo growth retardation and pregnancy loss during mid-gestation. Histological analysis of the Runx1-null uteri at gestation days 10-12 revealed an abnormally dense decidual tissue resulting from enhanced proliferation, impaired differentiation, and lack of apoptosis of stromal cells. The loss of Runx1 expression in uterine stromal cells also resulted in a marked impairment in the development of maternal blood vessels concomitant with a marked down regulation of several angiogenic factors, such as VEGF-A and angiopoietin-2. Furthermore, immunohistochemical analysis of smooth muscle actin and cytokeratin in the uterine sections of the mutant mice revealed a lack of maternal spiral artery modification and restricted trophoblast invasion. Collectively, these studies demonstrated that in the absence of Runx1 the decidua fails to produce critical factors that impact blood vessel formation, spiral artery modification, stromal apoptosis, and trophoblast migration. Thus, the Runx1-conditional knockout mouse presents an important animal model to study the molecular pathways that operate at the maternal-fetal interphase to control events that are critical for maintenance of pregnancy.","Item withdrawn by Mark Zulauf (zulauf@illinois.edu) on 2013-03-28T19:10:13Z Item was in collections: University of Illinois Theses & Dissertations (ID: 1) No. of bitstreams: 2 Athilakshmi_Kannan thesis final.docx: 81662150 bytes, checksum: dc8acc270ed1c6fcc257f17044eb2411 (MD5) Athilakshmi_Kannan.pdf: 3943258 bytes, checksum: db21a0dfd85da8c1be7d0d199faa55f9 (MD5)","Made available in DSpace on 2013-05-28T19:18:17Z (GMT). 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