TNF-α downregulates eNOS expression and mitochondrial biogenesis in fat and muscle of obese rodents
J. Clin. Invest. Alessandra Valerio, et al. 116:2791 doi:10.1172/JCI28570 [Go to this article.]

Figure 4
TNF-α signaling deficiency partly restores mitochondrial biogenesis in genetic obesity. (A) eNOS mRNA and protein levels were analyzed by quantitative RT-PCR or immunoblotting, respectively, in WAT of wild-type, ob/ob, ob/ob p55^–/–, ob/ob p75^–/–, and ob/ob p55^–/–p75^–/– mice. Relative values are mean ± SEM (n = 3 per group) when control measurements were assigned a value of 1.0. (B) PGC-1α, NRF-1, and Tfam mRNA were analyzed by means of quantitative RT-PCR with gene-specific oligonucleotide probes in WAT of wild-type, ob/ob, ob/ob p55^–/–, ob/ob p75^–/–, and ob/ob p55^–/–p75^–/– mice. The cycle number at which the various transcripts were detectable was compared with that of β-actin as an internal control and expressed as arbitrary units. (C) COX IV and Cyt c protein levels were detected by densitometric analysis of immunoblots in WAT of wild-type, ob/ob, ob/ob p55^–/–, ob/ob p75^–/–, and ob/ob p55^–/–p75^–/– mice. ***P < 0.01, *P < 0.05 versus wild-type (n = 3 per group); ^†P < 0.05 versus ob/ob.