Skip to main content
. Author manuscript; available in PMC: 2014 Jul 23.
Published in final edited form as: Circulation. 2013 Jun 19;128(4):10.1161/CIRCULATIONAHA.113.003183. doi: 10.1161/CIRCULATIONAHA.113.003183

Figure 8.

Figure 8

βAR desensitization by TNFα is GRK2 dependent (A) Representative tracings of isolated myocytes from GRK2 floxed mice (GRK2 f/f) or GRK2 knockout mice (GRK2 del) following pre-treatment with ISO or TNFα. (B & C) Cell-contractility measurements upon ISO in myocytes from GRK2 f/f or GRK2 del mice pre-treated with Veh, ISO or TNFα. *p < 0.01 versus ISO + ISO GRK2 f/f; #p < 0.01 versus TNFα + ISO GRK2 f/f (n =5, ~30 cells/experiment). (D) Plasma membrane from mouse aortic endothelial cells of Wt, TNFR1 or TNFR2 knock out mice (TNFR1−/− or TNFR2−/−) treated with Veh or TNFα were immunoblotted for phospho-β2AR. The blots were stripped and re-probed for GRK2 and β-actin. (E) TNFR1 was immunoprecipitated from cardiac lysates of Wt or TNFR2−/− mice and TNFR2 was immunoprecipitated from Wt or TNFR1−/− mice and immunoblotted for co-immunoprecipitating GRK2 (n=6). (F) Illustration depicting mechanism of TNFα-mediated desensitization of βAR through TNFR2 and GRK2.