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Figure 3 | Cell Communication and Signaling

Figure 3

From: GRK2 blockade with βARKct is essential for cardiac β2-adrenergic receptor signaling towards increased contractility

Figure 3

Levels of cardiac Bcl-2, NFκB activity and GRK5 post-MI. (A-B) Western blotting in total cardiac extracts from 24 hr post-MI B1KO and βARKct/B1KO (CT/B1KO) mice for βARKct, Bcl-2, phospho-IκBα (pIκBα), and total IκBα. Representative blots are shown in (A), including blots for glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as loading control for each protein tested, and densitometric quantitation, normalized with GAPDH as control and expressed as % of B1KO levels, of 4 independent experiments done in duplicate, is shown in (B). *, p<0.05, vs. B1KO. (C) Western blotting for Bcl-2 protein in total cardiac extracts from 4 week post-MI B1KO and βARKct/B1KO (CT/B1KO) mice. Representative blots from 4 independent experiments done in duplicate are shown, including GAPDH as loading control and h9c2 cell extract as positive control (input) for Bcl-2. Bcl-2 was virtually undetectable in either group at 4 weeks post-MI. (D) Western blotting for GRK5 in total cardiac extracts from B1KO and βARKct/B1KO (CT/KO) mice at 24 hrs and at 4 weeks (wks) post-MI. Representative blots of 4 independent experiments done in duplicate, with GAPDH as loading control, are shown on top, and densitometric quantitation on bottom. *, p<0.05, vs. all other groups.

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