The role of inhibitory κB kinase epsilon in model of aortic dissection

Abstract

Objective To study the role of inhibitory κB (IκB) kinase epsilon (IKKe) in angiotensin Ⅱ (AngⅡ)-induced aortic dissection formation in mice. Methods C57BL/6 mice were selected and divided into 2 groups: apolipoprotein E (ApoE)-/- group as control group, consisting of ApoE-knockout mice (ApoE-/-) subcutaneously infused by AngⅡ (AA group) and normal saline (AN group); ApoE-/- IKKe-/- group as experimental group, consisting of ApoE/IKKe-double knockout mice (ApoE-/- IKKe-/-) subcutaneously infused by AngⅡ (DA group) and normal saline (DN group). Changes in blood pressure, mortality rate, and aortic wall morphological changes of mice in every group were observed and recorded. Results Mice in AN and DN groups showed no obvious abnormal changes in blood pressure, no deaths, and no abnormal pathological changes in aortic wall structural integrity. Mice in both AA and DA groups showed elevated blood pressure and it was elevated more obviously in AA group (P=0.000) compared with in DA group; mice in AA group showed no deaths, whilst 4 mice died within a week in DA group (P=0.000); mice in both AA and DA groups showed different levels of pathological changes in aortic wall, but the aortic wall of mice in DA group were thickened, there were increased loss of smooth muscle in medial layer (the degree of deficiency in vessel wall of the mice in DA group versus AA group 4.50±1.12 vs. 1.50±0.93, P=0.000), and increased extracellular matrix degradation compared with those in AA group(degree of degradation of elastin in DA group versus AA group, 2.25±0.66 vs. 0.63±0.74, P=0.000). Conclusion IKKe deletion promoted aortic dissection formation induced by AngⅡ in mice of experimental group. Key words: Inhibitory κB kinase eplison; Angiotensin Ⅱ; Aortic dissection