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. 2021 Jan 13;10(1):146. doi: 10.3390/cells10010146

Figure 8.

Figure 8

Increased mitochondrial function after activation of β2-ARs is dependent on downstream Gαs-PKA signaling. Experimental design for pharmacological treatments in C2C12 myotubes (a), basal mitochondrial OCR (oxygen consumption ratio) (b), maximal mitochondrial OCR induced by FCCP (c), and ATP-independent OCR measured in the presence of oligomycin (d) in C2C12 myotubes acutely exposed to the non-selective β-AR agonist isoproterenol (ISO—1 µM for 30 min), with or without Gαi protein blockade with pertussis toxin (PTX—0.75 µg/mL, 3 h prior to ISO treatment). Basal mitochondrial OCR (e), maximal mitochondrial OCR induced by FCCP (f), and ATP-independent OCR measured in the presence of oligomycin (g) in C2C12 myotubes acutely exposed to the non-selective β-AR agonist isoproterenol (ISO—1 µM for 30 min), and/or under PKA blockade with PKI (20 µM, 30 min prior to ISO treatment). Data are presented as mean ± SE. * p < 0.05 vs. control and ** p < 0.05 vs. ISO. n = 9/group.