2015年第42卷第2期目录
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封面故事:血管重塑是众多心血管疾病的共同病理基础,迄今为止其形成机制尚不完全明确,目前的研究成果还没有形成有效的药物和器械以防止血管重塑的发生.E1A激活基因阻遏子(cellular repressor of E1A-stimulated genes,CREG)是1998年发现的参与维持组织细胞成熟分化稳态的内源性调控分子.韩雅玲研究组发现,在小鼠颈动脉损伤模型中CREG基因表达变化与病理性血管重塑程度呈负相关关系,血管损伤后CREG的表达为先迅速降低,再逐渐回升,而血管重塑程度则表现为持续加重,提示CREG基因参与血管损伤导致的病理性血管重塑过程,并可能决定了血管重塑的进程和结局.因此,血管损伤早期针对CREG基因进行有效干预,可能会抑制病理性血管重塑的发生发展.综上,CREG有可能成为防治血管重塑相关疾病的有效调控基因,为这类疾病的防治提供新的研究方向和干预靶点.
(李 洋,闫承慧,田孝祥,彭程飞,韩雅玲. E1A激活基因阻遏子基因表达变化与颈动脉血管重塑的关系,本期第161~168页)
Cover Story:Cellular repressor of E1A-stimulated genes (CREG) has been shown to be ubiquitously expressed in human and mouse tissues. However, its physiological functions and possible involvement in pathological processes remain unknown. To explore pathogenesis of vascular remodeling and possible role of CREG, we established an injury model of the mouse carotid artery in the present study. High-resolution small-animal ultrasound, Masson staining, immunohistochemistry, RT-PCR and Western-blot were used to detect the intima-media thickness, collagen content, the change of collagen typeⅠ and CREG expression of arterial wall at different time after arterial injury. CREG was expressed in normal arteries. The expression of CREG mRNA and protein of the arterial wall was markedly down-regulated after injury of mouse carotid artery, and reached its lowest value on the third day after arterial injury, with close correlation to the process of vascular remodeling (increase in mRNA and protein level of collagen typeⅠ). CREG expression was gradually restored on the seventh day, and almost returned to normal levels on fourteenth day and twenty-eighth day after arterial injury. In contrast, injured arteries developed marked vascular remodeling after 7 days as manifested by increase in intima-media thickness, narrowing of the vascular lumen, collagen content as well as mRNA and protein level of collagen typeⅠ. There were negative relationships between CREG expression and vascular remodeling at the early time of artery injuries. The expression of CREG was decreased at beginning and then increased, but the degree of vascular remodeling was continued to exacerbate. These data strongly suggest that CREG is involved in the development of vascular remodeling after arterial injury, and that injury-induced CREG down-regulation may contribute to the progression of vascular remodeling.
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综述与专论
研究报告
技术与方法
Letter to Editor
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