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炎症性肠病患者中血管内皮生长因子(VEGF)和CD146表达增加。

Increased expression of VEGF and CD146 in patients with inflammatory bowel disease.

作者信息

Tsiolakidou G, Koutroubakis I E, Tzardi M, Kouroumalis E A

机构信息

Departments of Gastroenterology and Pathology, University Hospital Heraklion, Crete, Greece.

出版信息

Dig Liver Dis. 2008 Aug;40(8):673-9. doi: 10.1016/j.dld.2008.02.010. Epub 2008 Apr 18.

Abstract

BACKGROUND

Angiogenesis has been suggested as an integral part of inflammatory bowel disease pathology. Vascular endothelial growth factor has long been considered to play a central, specific role in angiogenesis. Endothelial junction adhesion molecules, such as CD146, have recently been suggested to play a potent role in angiogenesis. CD34 is expressed on vascular endothelium, and it has been reported to be upregulated on endothelium in IBD. We investigated the expression of tissue vascular endothelial growth factor, CD34 and CD146 in the inflamed mucosa of patients with active inflammatory bowel disease compared with no inflamed mucosa of healthy controls.

METHODS

Forty-two IBD patients [23 ulcerative colitis, 19 Crohn's disease] and ten healthy controls were included in the study. In colonoscopically obtained biopsies, CD34, CD146 and vascular endothelial growth factor expression were evaluated by immunohistochemistry.

RESULTS

Vascular endothelial growth factor was detected in the mucosa of all groups, and its expression was significantly higher in both Crohn's disease and ulcerative colitis compared with controls (p<0.05). Immunohistochemical staining for CD146 in the inflamed mucosa was significantly higher in both Crohn's disease and ulcerative colitis compared with controls (p=0.002). A trend of higher CD34 expression in Crohn's disease and ulcerative colitis compared with controls was also found, but the difference among the three groups was not statistically significant (p=0.09).

CONCLUSIONS

Inflamed mucosa of patients with active Crohn's disease and ulcerative colitis showed a markedly enhanced expression of VEGF and CD146, than normal mucosa of controls, indicating a possible role of angiogenesis in the pathogenesis of inflammatory bowel disease.

摘要

背景

血管生成被认为是炎症性肠病病理学的一个重要组成部分。长期以来,血管内皮生长因子一直被认为在血管生成中发挥核心、特定的作用。内皮连接黏附分子,如CD146,最近被认为在血管生成中发挥重要作用。CD34在血管内皮细胞上表达,据报道在炎症性肠病的内皮细胞上表达上调。我们研究了活动性炎症性肠病患者炎症黏膜中组织血管内皮生长因子、CD34和CD146的表达,并与健康对照的非炎症黏膜进行比较。

方法

42例炎症性肠病患者[23例溃疡性结肠炎,19例克罗恩病]和10例健康对照纳入研究。通过结肠镜获取活检组织,采用免疫组织化学法评估CD34、CD146和血管内皮生长因子的表达。

结果

所有组的黏膜中均检测到血管内皮生长因子,与对照组相比,克罗恩病和溃疡性结肠炎中其表达均显著升高(p<0.05)。与对照组相比,克罗恩病和溃疡性结肠炎炎症黏膜中CD146的免疫组织化学染色均显著升高(p=0.002)。还发现与对照组相比,克罗恩病和溃疡性结肠炎中CD34表达有升高趋势,但三组间差异无统计学意义(p=0.09)。

结论

活动性克罗恩病和溃疡性结肠炎患者的炎症黏膜与对照组正常黏膜相比,VEGF和CD146表达明显增强,表明血管生成在炎症性肠病发病机制中可能起作用。

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