Lack of intracranial atherosclerosis in various atherosclerotic mouse models.

Vascular biology (Bristol, England) Pub Date : 2025-01-29 Print Date: 2025-01-01 DOI:10.1530/VB-23-0013
Diewertje I Bink, Katja Ritz, Claire Mackaaij, Olga Stam, Sanny Scheffer, Mark R Mizee, Hanneke J Ploegmakers, Bert J van Het Hof, Onno J de Boer, Judith C Sluimer, Guido R Y De Meyer, Louise van der Weerd, Helga E de Vries, Mat J A P Daemen
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Abstract

Although mice are used extensively to study atherosclerosis of different vascular beds, limited data are published on the occurrence of intracranial atherosclerosis. Since intracranial atherosclerosis is a common cause of stroke and is associated with dementia, a relevant animal model is needed to study these diseases. We examined the presence of intracranial atherosclerosis in different atherogenic mouse strains and studied differences in vessel wall characteristics in mouse and human tissue in search of possible explanations for the differing atherosclerotic susceptibility between extracranial and intracranial vessels. The presence of atherosclerotic plaques was systematically examined from the distal common carotids to the circle of Willis in three atherogenic mouse models. Extra- and intracranial vessel characteristics were studied by immunohistochemistry. All three strains developed atherosclerotic lesions in the common carotids, while no lesions were found intracranially. This coincided with altered vessel morphology. Compared to extracranial sections, intracranially the number of elastic layers decreased, tight junction markers increased, and antioxidant enzyme heme oxygenase (HO)-1 increased. Higher HO-1 expression was also shown in human intracranial arteries. Human brain endothelial cell stimulation with oxidized LDL induced endogenous protective antioxidant HO-1 levels through NRF2 translocation. Intracranial atherosclerosis was absent in three atherogenic mouse models. Intracranial vessel segments showed an increased presence of junction markers in mice and increased HO-1 in both mice and human tissue. We suggest that differences in brain vessel structure and induced antioxidant levels in the brain endothelium found in mouse and human tissue may contribute to the decreased atherosclerosis susceptibility of intracranial arteries.

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各种动脉粥样硬化小鼠模型缺乏颅内动脉粥样硬化。
背景:虽然小鼠被广泛用于研究不同血管床的动脉粥样硬化,但关于颅内动脉粥样硬化发生的数据有限。由于颅内动脉粥样硬化是卒中的常见原因,并与痴呆相关,因此需要建立相关的动物模型来研究这些疾病。方法和结果:我们在不同的致动脉粥样硬化小鼠品系中检测了颅内动脉粥样硬化的存在,并研究了小鼠和人体组织中血管壁特征的差异,以寻找颅内外血管和颅内血管之间不同的动脉粥样硬化易感性的可能解释。在三种动脉粥样硬化小鼠模型中,系统地检查了从总颈动脉远端到威利斯圈的动脉粥样硬化斑块的存在。免疫组织化学研究颅内外血管特征。所有三个品系均在总颈动脉中发生动脉粥样硬化病变,而颅内未发现病变。这与血管形态的改变相吻合。与颅外切片相比,脑组织弹性层数减少,紧密连接标记物增加,抗氧化酶血红素加氧酶(HO)-1升高。HO-1在人颅内动脉中也有较高表达。氧化低密度脂蛋白刺激人脑内皮细胞通过Nrf2易位诱导内源性保护性抗氧化剂HO-1水平。结论:3种动脉粥样硬化小鼠模型均无颅内动脉粥样硬化。颅内血管段在小鼠中显示出连接标记物的增加,在小鼠和人体组织中均显示出HO-1的增加。我们认为,小鼠和人类组织中发现的脑血管结构和诱导的脑内皮抗氧化水平的差异可能有助于降低颅内动脉粥样硬化的易感性。
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