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血管生成:特应性皮炎角蛋白14白细胞介素-4转基因小鼠模型的主要异常情况。

Angiogenesis: the major abnormality of the keratin-14 IL-4 transgenic mouse model of atopic dermatitis.

作者信息

Agha-Majzoub Rania, Becker Robert P, Schraufnagel Dean E, Chan Lawrence S

机构信息

Department of Dermatology, University of Illinois, Chicago, 60612, USA.

出版信息

Microcirculation. 2005 Sep;12(6):455-76. doi: 10.1080/10739680591003297.

DOI:10.1080/10739680591003297
PMID:16147464
Abstract

OBJECTIVE

Angiogenesis plays an important role in psoriasis, but its role in atopic dermatitis is unknown. The authors examined the dermal microvasculature of an IL-4 transgenic mouse model of atopic dermatitis to determine whether angiogenesis was present.

METHODS

Transmission and scanning electron microscopy and confocal microscopy studies were performed.

RESULTS

Transmission electron microscopy showed sprouting, transcapillary pillars of intussusception, thickened endothelial cells with large nuclei, and increased interendothelial junctional cleft number and length. Compared to nontransgenic littermates, there was a significant increase in the lengths and numbers of the interendothelial junctional clefts, along with a decrease in the length ratios of tight junction to interendothelial junctional clefts in both the early and late disease stages. In the early and late skin lesions, scanning electron microscopy of vascular corrosion casts showed disorganization of the capillary network hierarchy with increased density of capillary sprouts. Confocal microscopy of the animals with early and late skin lesions showed significant reduction in tight junction protein claudin-5.

CONCLUSIONS

Angiogenesis is the major pathologic feature in this model of atopic dermatitis. The chronic skin inflammation is intertwined with and may cause the angiogenesis, but the angiogenesis itself is likely to be important in this disease process.

摘要

目的

血管生成在银屑病中起重要作用,但其在特应性皮炎中的作用尚不清楚。作者检查了特应性皮炎白细胞介素-4转基因小鼠模型的真皮微血管,以确定是否存在血管生成。

方法

进行了透射电子显微镜、扫描电子显微镜和共聚焦显微镜研究。

结果

透射电子显微镜显示出芽、套叠式跨毛细血管柱、核大的内皮细胞增厚以及内皮细胞间连接裂隙数量和长度增加。与非转基因同窝小鼠相比,在疾病早期和晚期,内皮细胞间连接裂隙的长度和数量均显著增加,同时紧密连接与内皮细胞间连接裂隙的长度比降低。在早期和晚期皮肤病变中,血管铸型扫描电子显微镜显示毛细血管网络层次紊乱,毛细血管芽密度增加。对早期和晚期皮肤病变动物进行共聚焦显微镜检查显示紧密连接蛋白claudin-5显著减少。

结论

血管生成是该特应性皮炎模型的主要病理特征。慢性皮肤炎症与血管生成相互交织并可能导致血管生成,但血管生成本身在该疾病过程中可能很重要。

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