The mechanisms of Ang II-induced hypertensive vascular remodeling under suppression of CD68 in macrophages

Z.-G. Zhao, H.-F. Wang, Y.-W. Wang, J. Li, Y.-X. Li, H. Xin, J.-J. Liu, X.-M. Guan

Department of Vascular Surgery, The Affiliated Hospital of Qingdao University, Qingdao, China. jz1977vip@163.com

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• Cardiology

OBJECTIVE: High blood pressure (hypertension) is one of the most common cardiovascular diseases. In recent years, there were more and more studies on the function of inflammation in hypertension. CD68 mainly mediates the activation of cytokine interleukin-17 (IL-17) signaling pathway and participates in inflammatory responses. It has been studied the function of CD68 and IL-17 in hypertension, but it has not been reported whether it affected hypertension and vascular remodeling when macrophage CD68 expression inhibited. In this study, antisense-CD68 mice were used to study the effect and mechanism of angiotensin II-induced hypertensive vascular remodeling under specific suppression of macrophage CD68.

MATERIALS AND METHODS: Fifty 8-week-old male antisense-CD681 and C57 mice were divided into control and experimental group (angiotensin II group, 1000 ng•kg-1•min-1). After infusion of angiotensin II for 28 days, hematoxylin-eosin (HE) staining and immunohistochemical staining were used to observe the remodel of vascular. The changes of aortic inflammatory factors were detected by Real-time PCR (RT-PCR) and Western blotting.

RESULTS: By specifically inhibiting the expression of macrophage CD68, macrophage infiltration was mitigated in Ang II-induced hypertensive vascular remodeling model mouse, which also down-regulated the expression of vascular tissue inflammatory factor and activation of vascular smooth muscle cell p65.

CONCLUSIONS: CD68 regulates the Ang II-induced hypertensive vascular remodeling through mediating macrophage inflammatory factor release.

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