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Wnt3a/beta‐catenin increases proliferation in valve interstitial cells
Author(s) -
Xu Songyi,
Gotlieb Avrum
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1000.16
Subject(s) - wnt3a , wnt signaling pathway , cell growth , western blot , chemistry , beta catenin , interstitial cell , andrology , microbiology and biotechnology , biology , medicine , endocrinology , signal transduction , biochemistry , gene
Background Valve interstitial cells (VICs) mediate valve function in health and disease. It is suggested that valve repair processes are regulated by developmental pathways. We hypothesize that Wnt3a increases the amount of stabilized β‐catenin present in VICs, which then results in its nuclear translocation and subsequent increase in proliferation. Methods Porcine VIC cultures were maintained in standard media in 10% fetal bovine serum. Cultures were plated, grown to 4–6% confluence, then incubated with 100 ng/ml of exogenous Wnt3a for 3 days, and counted to measure proliferation. VICs were stained with antibody against β‐catenin. Whole cell, cytoplasmic and nuclear levels of β‐catenin were determined using Western blot. Results VICs treated with Wnt3a show increased cell number compared to control and vehicle‐treated cultures. Immunofluorescent images of Wnt3a‐treated VICs show slightly increased β‐catenin staining compare to control and vehicle‐treated cultures. Whole cell, cytoplasmic, and nuclear lysates of Wnt3a‐treated VICs show increased levels of β‐catenin compared to control and vehicle‐treated cultures. Conclusion Wnt3a may increase VIC proliferation through an increase in β‐catenin. Supported by the Heart and Stroke Foundation of Ontario (grant NA6204) and Canadian Institute of Health Research (grant 84228).