Ets-1 is a critical regulator of Ang II-mediated vascular inflammation and remodeling
J. Clin. Invest. Yumei Zhan, et al. 115:2508
doi:10.1172/JCI24403 [Go to this article.]

Figure 1
In vivo induction of Ets-1 in response to Ang II and altered vascular remodeling in Ets1–/– mice. (A) Ets-1 expression as measured by quantitative RT-PCR in the thoracic aorta of C57BL/6 mice, 3 days and 2 weeks after Ang II infusion (1.4 mg/kg/d). Values are expressed as fold induction compared with sham-treated controls. (B) Immunohistochemical analysis of Ets-1 expression after infusion of Ang II for 2 weeks in C57BL/6 mice compared with sham-treated controls. L, lumen. Original magnification, ×200. (C) Comparison of the effects of Ang II infusion and sham treatment on perivascular fibrosis and arterial thickening in the aorta of Ets1+/+ versus Ets1–/– mice. Aortic sections were stained with Masson trichrome stain. Original magnification, ×20 (left) and ×100 (right). (D) Analysis of medial thickness and medial area/lumen area ratio (left) and perivascular fibrosis thickness and fibrosis area/vessel area ratio (right) in Ets1+/+ versus Ets1–/– mice compared with sham-treated controls. (E) Comparison of the effect of Ang II infusion versus sham treatment on renal artery hypertrophy in Ets1+/+ versus Ets1–/– mice. Sections were stained with H&E. (F) Statistical analysis of medial thickness of the renal arteries in Ets1+/+ versus Ets1–/– mice compared with sham-treated controls. *P < 0.01 versus corresponding sham-treated control; P < 0.01 versus corresponding Ets1+/+ mice that underwent Ang II infusion. Values represent mean ± SEM; n = 5.