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Compared to healthy cells, <jats:styled-content style=\"fixed-case\">PAH PASMC<\/jats:styled-content>s demonstrate higher levels of proliferation both at baseline and with <jats:styled-content style=\"fixed-case\">PDGF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> that correlate with <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>3\u03b2 dependent \u03b2C activation. We show that \u03b2C knockdown but not Wnt5a stimulation reduces <jats:styled-content style=\"fixed-case\">PDGF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> dependent growth and normalizes <jats:styled-content style=\"fixed-case\">PAH PASMC<\/jats:styled-content>s proliferation. These findings support that cross\u2010talk between <jats:styled-content style=\"fixed-case\">PDGF<\/jats:styled-content> and Wnt signaling modulates <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content> proliferation and suggest that \u03b2C targeted therapies could treat abnormal vascular remodeling in <jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content>.<\/jats:p>","DOI":"10.1002\/1873-3468.12038","type":"journal-article","created":{"date-parts":[[2015,12,19]],"date-time":"2015-12-19T02:42:12Z","timestamp":1450492932000},"page":"101-109","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["<scp>PDGF<\/scp>\u2010dependent \u03b2\u2010catenin activation is associated with abnormal pulmonary artery smooth muscle cell proliferation in pulmonary arterial 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