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. Author manuscript; available in PMC: 2014 Feb 6.
Published in final edited form as: Hypertension. 2012 Jun 4;60(1):71–80. doi: 10.1161/HYPERTENSIONAHA.112.192500

Figure 3.

Figure 3

Effect of epidermal growth factor receptor (EGFR) kinase inhibition on EGFR expression, endothelial function, and endoplasmic reticulum (ER) stress markers in mesenteric resistance arteries (MRAs) from streptozotocin (STZ) mice. A, EGFR mRNA levels in all groups, n=5. B, Representative Western blot analysis and quantitative data for phosphorylated EGFR and total EGFR in all groups, n=3. C, Endothelium-dependent relaxation in response to acetylcholine (ACh) in MRA from control, STZ+AG1478, and STZ groups, n=5. D, Endothelium-independent relaxation in response to single nucleotide polymorphism in MRAs from all groups, n=5. ●, control; ×, STZ+AG1478; □, STZ. E, Representative Western blot analysis and quantitative data showing the phosphorylated endothelial NO synthase eNOS (P-eNOS) and total eNOS (T-eNOS), normalized to β-actin, in MRAs from all groups, n=4. F, Cyclic GMP levels in all the groups, n=4. G through J, Representative Western blot analysis showing the expression of phosphorylated eIF2-α, normalized to β-actin; total eIF2-α, n=4; and ATF-4, CHOP, and ATF-6 mRNA levels, normalized to 18S rRNA, in all groups, n=5. *P<0.05 for STZ vs control, #P<0.05 for STZ vs STZ+AG1478, and $P<0.05 for STZ+AG1478 vs control.