Knockout of Vdac1 activates hypoxia-inducible factor through reactive oxygen species generation and induces tumor growth by promoting metabolic reprogramming and inflammation

Table 1 Respiratory control of Wt and Vdac1 ^−/− MEF

	Nx		Hx
	Wt MEF	Vdac1 ^−/− MEF	Wt MEF	Vdac1 ^−/− MEF
(a) Basal respiration	20.52 ± 2.5	16.19 ± 1.8	4.5 ± 0.52	10.4 ± 2.41
(b) Oligomycin-insensitve respiration (leak)	5.96 ± 0.9	5.04 ± 0.9	2.4 ± 0.27	7.1 ± 2.73
(c) Oligomycin-sensitive (ATP turnover) respiration	14.56 ± 1.6	11.16 ± 0.8	1.8 ± 0.70	3.2 ± 0.95
(d) Maximal respiration in the presence of FCCP	29.21 ± 3.2	19.29 ± 1.7	5.4 ± 1.19	6.0 ± 0.29
(c/a) Coupling efficiency	0.71 ± 0.02	0.71 ± 0.01	0.4 ± 0.12	0.3 ± 0.13
(d/b) Respiratory control ratio	4.91 ± 0.2	3.95 ± 0.4	2.3 ± 0.71	0.8 ± 0.44
(d-a) Spare respiratory capacity	8.19 ± 1.2	3.10 ± 0.1	1.3 ± 0.50	−5.4 ± 2.83

The oxygen consumption rate (OCR) was measured in real time with a Seahorse XF bioenergetic system for Wt and Vdac1 ^−/−MEF in Nx or Hx. The average OCR was calculated from at least four measurements during treatment with each compound (oligomycin, FCCP, rotenone/antimycin A) at a 1 μM final concentration.
(a) represents basal respiration, (b) oligomycin-insensitive respiration, (c) oligomycin-sensitive respiration, and (d) maximal respiration in the presence of FCCP. The graph shows how to define a, b, c, and d. The mean ± SEM is representative of six independent experiments carried out in quadruplicate

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