Guangdong Institute of Gastroenterology, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Dig Dis Sci. 2018 Jan;63(1):113-125. doi: 10.1007/s10620-017-4818-1. Epub 2017 Oct 27.
Chronic radiation proctitis (CRP), a common complication after radiotherapy for pelvic malignancies, compromises patient quality of life. Vascular damage and aberrant angiogenesis in the mucosal layer are essential histological features, but changes to the submucosal layer are unclear. Thus, we evaluated the histological characteristics and distribution changes of key angiogenic factors in full-layered human CRP samples.
Thirty paraffin-embedded CRP and twenty-nine non-CRP tissues were used to evaluate histopathological changes. Immunohistochemistry with anti-CD34 antibody was performed to calculate microvascular density (MVD). Frozen tissues from eight CRP patients and five non-CRP controls were collected and analyzed by antibody array, which contained sixty human angiogenesis-related factors. Quality controls with positive and negative controls were performed during antibody array analysis. Two differentially expressed factors were confirmed by ELISA.
CRP lesions showed vasculopathy, fibrosis, mucosal ulceration, edema, and inflammatory cell infiltration. Human angiogenesis antibody array and ELISA confirmed the increased angiostatin in CRP lesions. Immunohistochemical staining showed dispersed distribution of angiostatin throughout the mucosal and submucosal layers in CRP lesions, while angiostatin accumulated within the vessel lumens in non-CRP tissues. MVD significantly decreased in the submucosal layer of CRP, suggesting a potential association with increased angiostatin.
Angiostatin increased and had a distinct distribution in CRP lesions. Compensatory telangiectasia in the mucosa, vessel stenosis, and reduced MVD might attenuate blood flow in the submucosa and contribute to CRP progression. Restoration of vascular functionality by promoting angiogenesis in the submucosal layer may help alleviate CRP in clinical practice.
慢性放射性直肠炎(CRP)是盆腔恶性肿瘤放疗后的常见并发症,会影响患者的生活质量。黏膜层的血管损伤和异常血管生成是其重要的组织学特征,但黏膜下层的变化尚不清楚。因此,我们评估了全层人 CRP 样本中关键血管生成因子的组织学特征和分布变化。
使用 30 例石蜡包埋的 CRP 和 29 例非 CRP 组织评估组织病理学变化。采用抗 CD34 抗体免疫组化法计算微血管密度(MVD)。收集 8 例 CRP 患者和 5 例非 CRP 对照者的冷冻组织,采用含有 60 个人类血管生成相关因子的抗体芯片进行分析。在抗体芯片分析过程中进行了阳性和阴性对照的质量控制。通过 ELISA 确认了两种差异表达的因子。
CRP 病变表现为血管病变、纤维化、黏膜溃疡、水肿和炎症细胞浸润。人血管生成抗体芯片和 ELISA 证实 CRP 病变中血管抑素增加。免疫组织化学染色显示 CRP 病变中血管抑素在黏膜和黏膜下层呈弥散性分布,而非 CRP 组织中血管抑素则积聚在血管腔内。CRP 患者的黏膜下层 MVD 显著降低,提示其与血管抑素的增加有关。
CRP 病变中血管抑素增加且分布不同。黏膜的代偿性毛细血管扩张、血管狭窄和 MVD 降低可能会减弱黏膜下层的血流,从而导致 CRP 的进展。通过促进黏膜下层的血管生成来恢复血管功能可能有助于在临床上缓解 CRP。