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. Author manuscript; available in PMC: 2015 Jan 16.
Published in final edited form as: J Mol Cell Cardiol. 2013 Dec 17;67:86–93. doi: 10.1016/j.yjmcc.2013.12.005

Fig. 4.

Fig. 4

Inhibition of p38α enhances phosphorylation of inhibitor-1 at Thr35. Immunoblot analyses of Ser67 (A) and Thr35 (B) I-1 phosphorylation in NRVMs, infected either with dn-p38α or dn-p38β, LacZ as control. Virus dose was 2 MOI in each well. C, Immunoblot of Thr35 I-1 phosphorylation in NRVMs, silenced either with negative control or p38α siRNA (150 nM). D, Immunoblot analysis of I-1 Thr35 phosphorylation in NRVMs infected either with LacZ (control) or wtGRK2 (2 MOI), treated with SB203580 (10 μM). E, Immunoblot analyses of Ser67 and Thr35 I-1 phosphorylation in Langendorff perfused hearts, treated either with vehicle, SB203580 (3 μM), ET-1 (3 nM) or SB203580 + ET-1 (3 μM + 3 nM) for 10 min. At the end of the experiment, total protein was extracted from left ventricular tissue samples. GAPDH as loading control for all western blots. I-1, inhibitor-1; NRVM, neonatal rat ventricular myocyte; ET-1, endothelin-1 ; dn-p38α/β, dominant negative p38α/β; PLB, phospholamban; GRK2, G-protein coupled kinase-2; wtGRK2, wild type GRK2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.