Figure 3
From: TAK1 Regulates Myocardial Response to Pathological Stress via NFAT, NFκB and Bnip3 Pathways
TAK1 regulates cardiomyocyte hypertrophy through NFAT and NFκB.
(A) Surface areas of cardiomyocytes infected with β-gal or TAK1ΔN adenoviruses, followed by stimulation with vehicle control (Con), phenylephrine (PE, 50 μmol/L), or angiotensin II (AngII, 100 nmol/L) for 24 h. *P < 0.01 versus Con Ad-βgal; #P < 0.05 versus Con Ad-TAK1ΔN. (B,C) NFAT-luciferase and NFκB-luciferase activity in cardiomyocytes infected with adenoviruses expressing NFAT-luciferase reporter along with β-gal or TAK1ΔN, followed by stimulation with vehicle control, PE, or AngII. *P < 0.05 versus Con Ad-β-gal; #P < 0.05 versus Ad-TAK1ΔN. (D) NFAT-luciferase activity in cardiomyocytes infected with adenoviruses expressing NFAT-luciferase reporter along with β-gal, TAK1ΔN, IκBαM, or dnIKKβ. *P < 0.01 versus None Ad-βgal; #P < 0.05 versus None Ad-TAK1ΔN. (E) NFκB-luciferase activity in cardiomyocytes infected with adenoviruses expressing NFκB-luciferase reporter along with β-gal, TAK1ΔN, Cain or Rcan1. *P < 0.01 versus None Ad-βgal; #P < 0.05 versus None Ad-TAK1ΔN. (F) Surface areas of cardiomyocytes infected with βgal, TAK1ΔN, TAK1 plus TAB1 adenoviruses along with Cain or IκBαM. *P < 0.05 versus None Ad-βgal; #P < 0.05 versus None Ad-TAK1ΔN or None TAK1 plus TAB1. (G) Schematic representation of the TAK1-activated hypertrophic signaling pathway.
