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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: J Endocrinol. 2019 Aug;242(2):159–172. doi: 10.1530/JOE-19-0126

Figure 6. Improved HFD-induced endothelial dysfunction in EC Adk-deficient mice.

Figure 6.

A. Representative images of immunofluorescence staining for isolectin GS-IB4 (left) and quantification of vessel density (middle) and AACC (adipogenic/angiogenic cell cluster) numbers (right) in epididymal WAT from AdkWT and AdkΔVEC mice after 12 weeks of HFD (n = 8 mice per group). B. Representative Western blot results of phospho-Nos3 (Ser1176) (p-Nos3S1176), total Nos3 (Nos3) and β-actin (left) from epididymal WAT in AdkWT and AdkΔVEC mice after 12 weeks of HFD. Relative ratio of p-Nos3S1176/β-actin (middle) and Nos3/β-actin (right) in epididymal WAT were quantitated by densitometric analysis of the corresponding Western blots (n = 6 mice per group). C. Relaxations of skeletal muscle arterioles in response to cumulative concentrations of acetylcholine (ACh) in the absence or presence of Nω-nitro-l-arginine methyl ester hydrochloride (L-NAME). Arterioles were isolated from AdkWT and AdkΔVEC mice after 12 weeks of HFD (n = 5–7 mice per group). All data are represented as mean ± SEM, *P < 0.05 and **P < 0.01 for AdkΔVEC vs. AdkWT (unpaired two-tailed Student’s t test).