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. Author manuscript; available in PMC: 2019 Aug 1.
Published in final edited form as: J Mol Cell Cardiol. 2018 Jul 21;121:205–211. doi: 10.1016/j.yjmcc.2018.07.130

Figure 5 – Differential potency of fibroblast- and cardiomyocyte-derived CCN2.

Figure 5 –

(A) qPCR analysis for α-Sma mRNA expression following intracellular CCN2 overexpression (intracell) or treatment with CCN2 exogenously provided in the media (extracell) on mouse embryonic fibroblasts (MEFs). Control (ctrl) is βGal overexpression or media from βGal overexpressing MEFs. n≥ 3 biological replicates / condition. (B) Representative immunofluorescence images for alpha smooth muscle actin (αSMA) (green) and nuclei (DAPI; blue). Scale bar is 100μm. (C) Quantification of αSMA protein expression using ImageJ NIH software and represented relative to control. n≥ 400 cells / condition. (D) Western blot for CCN2 presence in media derived from fibroblasts (fibro.) or cardiomyocytes (card.) treated with Ad-βGal (ctrl) or Ad-CCN2. Ponceau staining (bottom panel) indicates loading control. (E) qPCR analysis for α-Sma mRNA expression following stimulation of MEFs with conditioned media (CM) from fibroblasts (fibro.CM) or cardiomyocytes (card.CM). n≥ 3 biological replicates / condition. (F) Representative immunofluorescence images for alpha smooth muscle actin (αSMA) (green) and nuclei (DAPI; blue). Scale bar is 100μm. (G) Quantification of αSMA protein expression using ImageJ NIH software and represented relative to control. n≥400 cells / condition. *p<0.05 vs. ctrl; #p<0.05 vs. fibro.CM.