Skip to main content
. Author manuscript; available in PMC: 2012 Aug 1.
Published in final edited form as: Arthritis Rheum. 2011 Aug;63(8):2473–2483. doi: 10.1002/art.30317

Figure 4. Effect of kinase inhibitors on TGF-β1-induced α-SMA and Snail-1 expression in primary pulmonary EC.

Figure 4

Primary pulmonary EC were treated with either 5μM p38 MAP kinase inhibitor SB 203580, 1μM JNK MAP kinase inhibitor SP 600125, or 5μM Erk1/2 specific upstream inhibitor PD 98059 (A), or with 5μM PI3-kinase3 inhibitor LY294002 or 0.5μM PKC-δ inhibitor rottlerin (B) in the presence or absence of TGF-β1 for 72 h, then cell lysates were probed in Western blots for α-SMA. GAPDH was used as loading control. Note that SB 203580 and SP 600125 decrease TGF-β1-induced α-SMA expression, treatment with the PKC-δ inhibitor rottlerin almost completely abolished TGF-β1-induced α-SMA expression, whereas treatment with either the Erk1/2 inhibitor or the PI-3 kinase inhibitor had no significant effects. The quantitative densitometry of α-SMA was analyzed using NIH Image J software and the data represent one of two independent experiments *p < 0.05 when compared with the TGF-β1-treated group.