Male and female C57BL/6 mice (33 male and 10 female mice), males deficient in NADPH oxidase 1 (Nox1−/−, gift from Dr. DW. Stepp, Vascular Biology Center, Augusta University) (N=8), C‐C chemokine receptor type 5 (CCR5−/− mice, B6.129P2‐Ccr5tm1Kuz/J Jackson Laboratory) (N=8), and males with selective deletion of either Ptp1b (protein tyrosine phosphatase 1B) (N=7) or leptin receptor (LepR) (N=7), in endothelial cells (EC) have been used at 8 to 14 weeks of age. Inducible endothelial Ptp1b‐ and LepR‐deficient mice have been generated by crossing Cdh5‐CreERT2 mice (from R. Adams, Max‐Planck‐Institute) with Ptp1bflox/flox and LepRflox/flox, respectively (Jackson Laboratory). Endothelial‐specific deletion of Ptp1b or LepR was induced via activation of the endothelial‐specific Cre recombinase in 6‐ to 8‐week‐old mice by 5 for Ptp1b or 14 for LepR consecutive daily intraperitoneal injections of tamoxifen (0.1 mL of a 20 mg/mL solution in corn oil).24 , 25 Animals receiving tamoxifen injections (−/−) were compared with vehicle (corn oil)‐treated animals (+/+).
All animals were fed standard mouse chow, and tap water was provided ad libitum. Mice were housed in an American Association of Laboratory Animal Care–approved animal care facility at Augusta University. Augusta University Institutional Animal Care and Use Committee approved all protocols (IACUC protocol #2011‐0108).
All animals were fed standard mouse chow, and tap water was provided ad libitum. Mice were housed in an American Association of Laboratory Animal Care–approved animal care facility at Augusta University. Augusta University Institutional Animal Care and Use Committee approved all protocols (IACUC protocol #2011‐0108).