Deletion of the FHL2 gene attenuates the formation of atherosclerotic lesions after a cholesterol-enriched diet

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• 作者：Pao-Hsien Chu ; Hung-I Yeh ; Hsueh-Hua Wu ; Ray-Ching Hong ; Tzu-Fang Shiu ; Chuen-Mao Yang
• 关键词：Gap junctions ; Connexins ; Endothelial cells ; Nitrate ; Hyperlipidemia ; FHL2
• 刊名：Life Sciences
• 出版年：2010
• 出版时间：27 February 2010
• 年：2010
• 卷：86
• 期：9-10
• 页码：365-371
• 全文大小：4916 K

文摘

Aims

FHL2, a member of the four and a half LIM domain (FHL) family of proteins, may play an important role in the circulatory system and in particular atherosclerosis.

Main methods

To investigate the role of FHL2 in atherogenesis, FHL2-null and wild-type control male mice were fed either a normal chow (NC) or a cholesterol-enriched diet (CED).

Key findings

At 3 months post CED, aortic atherosclerotic plaques were observed in both control and FHL2-null mice. Lesions in control mice increased dramatically by 6 months of CED. In contrast, lesion size did not increase during this time in CED-fed FHL2-null mice. Relative to control mice on a normal chow of diet (NCD), control mice on a CED exhibited lower circulating nitric oxide (NO) levels, and decreased expression of connexin37 (Cx37) and Cx40 in aortic endothelium. In contrast, FHL2-null mice on a CED maintained similar levels of circulating NO as FHL2-null mice fed a NCD. Cxs levels in aortic endothelium of FHL2-null mutants on a NCD were lower relative to control mice on a NCD, and did not decrease with CED.

Significance

Our data demonstrate a role for FHL2 in atherogenesis, the regulation of circular NO release, and expression of gap junctions within aortic endothelium.