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Despite its frequent occurrence, the precise aetiology and physiopathology of adenomyosis is still unknown.\n                    <jats:styled-content style=\"fixed-case\">WNT<\/jats:styled-content>\n                    \/\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin signalling molecules are important and should be tightly regulated for uterine function. To investigate the role of\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin signalling in adenomyosis, the expression of\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin was examined. Nuclear and cytoplasmic\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin expression was significantly higher in epithelial cells of human adenomyosis compared to control endometrium. To determine whether constitutive activation of\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin in the murine uterus leads to development of adenomyosis, mice that expressed a dominant stabilized\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin in the uterus were used by crossing\n                    <jats:styled-content style=\"fixed-case\">PR<\/jats:styled-content>\n                    \u2010Cre mice with\n                    <jats:italic>\n                      Ctnnb1\n                      <jats:sup>f(ex3)\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice. Uteri of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">\n                        PR\n                        <jats:sup>cre<\/jats:sup>\n                      <\/jats:styled-content>\n                      <jats:sup>\/+<\/jats:sup>\n                      Ctnnb1\n                      <jats:sup>f(ex3)\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice displayed an abnormal irregular structure and highly active proliferation in the myometrium, and subsequently developed adenomyosis. Interestingly, the expression of E\u2010cadherin was repressed in epithelial cells of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">\n                        PR\n                        <jats:sup>cre<\/jats:sup>\n                      <\/jats:styled-content>\n                      <jats:sup>\/+<\/jats:sup>\n                      Ctnnb1\n                      <jats:sup>f(ex3)\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice compared to control mice. Repression of E\u2010cadherin is one of the hallmarks of epithelial\u2013mesenchymal transition (\n                    <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>\n                    ). The expression of\n                    <jats:styled-content style=\"fixed-case\">SNAIL<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">ZEB1<\/jats:styled-content>\n                    was observed in some epithelial cells of the uterus in\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">\n                        PR\n                        <jats:sup>cre<\/jats:sup>\n                      <\/jats:styled-content>\n                      <jats:sup>\/+<\/jats:sup>\n                      Ctnnb1\n                      <jats:sup>f(ex3)\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice but not in control mice. Vimentin and\n                    <jats:styled-content style=\"fixed-case\">COUP\u2010TFII<\/jats:styled-content>\n                    , mesenchymal cell markers, were expressed in some epithelial cells of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">\n                        PR\n                        <jats:sup>cre<\/jats:sup>\n                      <\/jats:styled-content>\n                      <jats:sup>\/+<\/jats:sup>\n                      Ctnnb1\n                      <jats:sup>f(ex3)\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice. In human adenomyosis, the expression of E\u2010cadherin was decreased in epithelial cells compared to control endometrium, while\n                    <jats:styled-content style=\"fixed-case\">CD10<\/jats:styled-content>\n                    , an endometrial stromal marker, was expressed in some epithelial cells of human adenomyosis. These results suggest that abnormal activation of\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010catenin contributes to adenomyosis development through the induction of\n                    <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>\n                    . Copyright \u00a9 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.4224","type":"journal-article","created":{"date-parts":[[2013,6,19]],"date-time":"2013-06-19T13:50:36Z","timestamp":1371649836000},"page":"210-222","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":93,"title":["<i>\u03b2<\/i>\n                    \u2010Catenin activation contributes to the pathogenesis of adenomyosis through epithelial\u2013mesenchymal transition"],"prefix":"10.1002","volume":"231","author":[{"given":"Seo Jin","family":"Oh","sequence":"first","affiliation":[{"name":"Department of Obstetrics, Gynecology and Reproductive Biology Michigan State University, College of Human Medicine Grand Rapids MI 49503 USA"},{"name":"WCU Biomodulation Major College of Agriculture and Life Sciences, Seoul National University Seoul 151\u2010742 Republic of 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