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. Author manuscript; available in PMC: 2012 Feb 15.
Published in final edited form as: Circulation. 2011 Jan 31;123(6):584–593. doi: 10.1161/CIRCULATIONAHA.110.971853

Figure 6. EPA and DHA inhibit the TGF-β1-stimulated fibrotic response through the cGMP/PKG pathway.

Figure 6

(A) cGMP levels measured by ELISA in cultured cardiac fibroblasts treated for 48 hr with EPA and DHA (10–50 μM), using AA (10–20 μM), and OA (10–20 μM) (n=3–7) as control. (B) Collagen synthesis determined by [3H]-proline incorporation in cardiac fibroblasts treated for 48 hr with EPA (10 μM), DHA (10 μM), 8-bromo-cGMP (1 mM), and/or the guanylyl cyclase inhibitor DT-3 (1 μM) and for the final 24 hr with TGF-β1 (1 ng/ml) (n=4–20). (C) Smad2 and Smad3 phosphorylation (Smad2 Ser465/467; Smad3 Ser423/425) detected by Western blot in cultured cardiac fibroblasts treated for 24 hr with EPA or DHA (10 μM) and for an additional 30 min or 24 hr with fatty acids and TGF-β1 (1 ng/ml). (D, E) Quantification of Smad2 or Smad3 phosphorylation relative to total Smad2/3 (n=3). Data are presented as mean ± SEM. Means were compared by each pair Student t test in B, one-way ANOVA with Dunnet’s post-hoc test in A and Tukey’s post-hoc test in D, E.