Additional Supporting Information may be found in the online version of this article.

sc-12-0845_sm_SupplTabe1.pdf18KSupplementary Table 1
sc-12-0845_sm_SupplText.pdf107KSupplementary Data
sc-12-0845_sm_SupplFigure1.TIF1588KFigure S1. hnRNPA1 is specific for SMC differentiation from ES cells on collagen IV. ES cells cultured on collagen IV were transfected with pCMV-hnRNPA1 or empty vector control pCMV5 (1μg/106 cells) (A), or random control siRNA or hnRNPA1 siRNA (B), respectively. The cells were harvested and subjected to real-time RT-PCR analysis with sets of primers specific for different cell lineages genes: Flt-1 and CD144 for endothelial, Ddr2 and Thy1 for cardiac fibroblast, Tnnc 1 and actc1 for cardiac myocytes, Alcam and CD133 for hematopoietic progenitor, Dlx3 and Tpbg for trophoblast, CD29 and CD44 for mesenchymal, nestin and Gap43 for neural. The data are means±S.E.M of three independent experiments.
sc-12-0845_sm_SupplFigure2.TIF1911KFigure S2. Knockdown hnRNPA1 reduces calponin-positive SMCs derived from stem cells in vivo. Frozen sections from implants were subjected to double immunofluorescence staining with antibodies against beta-galactosidase (β-gal) and SMC marker calponin. The total numbers of Calponin-positive cells per field were counted by two well-trained independent investigators blinded to the treatments, from four random high power fields (200x) in each section, two sections from each implant and five implants for each group. Representative images (top panels) and quantitative data (bar graphs) were presented here. *p< 0.05.
sc-12-0845_sm_SupplFigure3.TIF1366KFigure S3 Schematic illustration of Acta2 (A) and Tagln (B) gene promoter regions.
sc-12-0845_sm_SupplFigure4.TIF1538KFigure S4 Schematic illustration of SRF (A), MEF2c (B) and Myocd (C) gene promoter regions. The number within the promoter region was defined according to its position with the start condon (‘A’: +1) of respective genes. Black region in respective gene represents the promoter we used in this study.

Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.