Boston, Mass. From the Departments of Plastic and Oral Surgery and Surgery, Vascular Anomalies Center, Vascular Biology Program, Children's Hospital Boston, Harvard Medical School.
Plast Reconstr Surg. 2011 Oct;128(4):260e-269e. doi: 10.1097/PRS.0b013e3182268afd.
ACKGROUND:: Arteriovenous malformations cause significant morbidity, primarily because they expand over time and recur after treatment. The authors hypothesized that neovascularization might contribute to arteriovenous malformation progression.
Arteriovenous malformation tissue was collected prospectively from 12 patients after resection. Schobinger stage was determined by clinical history. Neovascularization in stage II lesions (n=7) was compared with stage III arteriovenous malformations (n=5) that had progressed. Specimens were analyzed using immunohistochemistry for CD31, Ki67, and CD34/CD133. Quantitative real-time reverse-transcriptase polymerase chain reaction was used to determine mRNA expression of factors that recruit endothelial progenitor cells: vascular endothelial growth factor (VEGF), stromal cell-derived factor-1α (SDF-1α), and hypoxia-inducible factor-1α (HIF-1α). VEGF receptors (VEGFR1, VEGFR2, neuropilin 1, and neuropilin 2) also were quantified using quantitative real-time reverse-transcriptase polymerase chain reaction.
Stage III arteriovenous malformations showed greater microvessel density (5.8 percent) than stage II lesions (1.3 percent) (p=0.004); no difference in proliferating endothelial cells was noted (p=0.67). CD133CD34 endothelial progenitor cells were elevated in stage III (0.53 percent) compared with stage II arteriovenous malformations (0.25 percent) (p=0.03). HIF-1α and SDF-1α were increased 7.6- and 7.9-fold in stage III compared with stage II lesions (1.7-fold and 3.3-fold), respectively (p=0.02). Neuropilin 1 and neuropilin 2 expression was greater in stage III (5.8-fold and 4.6-fold) than stage II arteriovenous malformations (3.0-fold and 2.4-fold) (p=0.03).
Higher-staged arteriovenous malformations exhibit increased expression of endothelial progenitor cells and factors that stimulate their recruitment. Neovascularization by vasculogenesis may be involved in progression of arteriovenous malformation.
动静脉畸形会导致严重的发病率，主要是因为它们会随着时间的推移而扩张，并在治疗后复发。作者假设血管新生可能有助于动静脉畸形的进展。
从 12 名患者的动静脉畸形切除术后前瞻性采集组织。Schobinger 分期由临床病史确定。比较了 II 期病变（n=7）的血管新生与进展的 III 期动静脉畸形（n=5）。使用免疫组织化学法检测 CD31、Ki67 和 CD34/CD133。使用定量实时逆转录聚合酶链反应测定招募内皮祖细胞的因子的 mRNA 表达：血管内皮生长因子（VEGF）、基质细胞衍生因子-1α（SDF-1α）和缺氧诱导因子-1α（HIF-1α）。还使用定量实时逆转录聚合酶链反应定量测定 VEGF 受体（VEGFR1、VEGFR2、神经钙蛋白 1 和神经钙蛋白 2）。
III 期动静脉畸形的微血管密度（5.8%）明显高于 II 期病变（1.3%）（p=0.004）；增殖的内皮细胞无差异（p=0.67）。III 期 CD133CD34 内皮祖细胞（0.53%）高于 II 期动静脉畸形（0.25%）（p=0.03）。与 II 期病变相比，III 期 HIF-1α 和 SDF-1α 分别增加了 7.6 倍和 7.9 倍（1.7 倍和 3.3 倍）（p=0.02）。与 II 期动静脉畸形相比，III 期神经钙蛋白 1 和神经钙蛋白 2 的表达更高（5.8 倍和 4.6 倍）（p=0.03）。
更高分期的动静脉畸形表现出内皮祖细胞及其募集刺激因子的表达增加。血管生成的血管新生可能参与动静脉畸形的进展。
