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. Author manuscript; available in PMC: 2010 May 1.

Published in final edited form as: J Mol Cell Cardiol. 2009 Jan 21;46(5):621–635. doi: 10.1016/j.yjmcc.2009.01.005

C3H10T1/2 cells were treated for 4 days with either vehicle, 15 ng/ml Wnt3a, 5 ng/ml TGFβ₁, and/or 100 ng/ml BMP2 in the combinations indicated. Total cellular RNA was extracted and gene expression analyzed by RT-qPCR as described in “Materials and Methods.” Wnt5a (15 ng/ml) was unable to replace Wnt3a actions in this assay (data not shown). Panel B, quantitative western blot analysis confirms that Wnt3a is capable of significantly augmenting SM22α protein accumulation in either the presence or absence of TGFβ₁. Data were obtained from quantitative image analysis of 4 independent replicates following 4 days of the indicated treatments, normalizing the SM22α signal to eIF2alpha signal in each sample.

C3H10T1/2 cells were treated for 4 days with either vehicle, 15 ng/ml Wnt3a, 5 ng/ml TGFβ₁, and/or 100 ng/ml BMP2 in the combinations indicated. Total cellular RNA was extracted and gene expression analyzed by RT-qPCR as described in “Materials and Methods.” Wnt5a (15 ng/ml) was unable to replace Wnt3a actions in this assay (data not shown). Panel B, quantitative western blot analysis confirms that Wnt3a is capable of significantly augmenting SM22α protein accumulation in either the presence or absence of TGFβ₁. Data were obtained from quantitative image analysis of 4 independent replicates following 4 days of the indicated treatments, normalizing the SM22α signal to eIF2alpha signal in each sample.