Hellenic Centre of Neurosurgical Research "Professor Petros S. Kokkalis", University of Athens, Athens, Greece.
J Neurosurg. 2013 Feb;118(2):353-7. doi: 10.3171/2012.10.JNS12327. Epub 2012 Nov 9.
A considerable body of evidence indicates that inflammation and angiogenesis play a significant role in the development and progression of chronic subdural hematoma (CSDH). While various experimental and clinical studies have implicated placental growth factor (PlGF) in the processes that underpin pathological angiogenesis, no study has thus far investigated its expression in CSDH. The actions of PlGF and its related proangiogenic vascular endothelial growth factor (VEGF) are antagonized by a high-affinity soluble receptor, namely soluble VEGF receptor-1 (sVEGFR-1), and thus the ratio between sVEGFR-1 and angiogenic factors provides an index of angiogenic capacity.
In the present study, using an automated electrochemiluminescence assay, levels of PlGF and sVEGFR-1 were quantified in serum and hematoma fluid obtained in 16 patients with CSDH.
Levels of PlGF and sVEGFR-1 were significantly higher in hematoma fluid than in serum (p < 0.0001). In serum, levels of sVEGFR-1 were higher than those of PlGF (p < 0.0001), whereas in hematoma fluid this difference was not apparent. Furthermore, the ratio of sVEGFR-1 to PlGF was significantly lower in hematoma fluid than in serum (p < 0.0001).
Given previous evidence indicating a role for PlGF in promoting angiogenesis, inflammatory cell chemotaxis, and stimulation, as well as its ability to amplify VEGF-driven signaling under conditions favoring pathological angiogenesis, enhanced expression of PlGF in hematoma fluid suggests the involvement of this factor in the mechanisms of inflammation and angiogenesis in CSDH. Furthermore, a reduced ratio of sVEGFR-1 to PlGF in hematoma fluid is consistent with the proangiogenic capacity of CSDH. Future studies are warranted to clarify the precise role of PlGF and sVEGFR-1 in CSDH.
大量证据表明，炎症和血管生成在慢性硬脑膜下血肿（CSDH）的发展和进展中起着重要作用。虽然各种实验和临床研究表明胎盘生长因子（PlGF）在支持病理性血管生成的过程中，但迄今为止尚无研究调查其在 CSDH 中的表达。PlGF 及其相关的促血管生成血管内皮生长因子（VEGF）的作用被高亲和力可溶性受体，即可溶性 VEGF 受体-1（sVEGFR-1）拮抗，因此 sVEGFR-1 和血管生成因子之间的比例提供了血管生成能力的指标。
在本研究中，使用自动化电化学发光测定法，定量测定了 16 例 CSDH 患者血清和血肿液中的 PlGF 和 sVEGFR-1 水平。
血肿液中的 PlGF 和 sVEGFR-1 水平明显高于血清（p <0.0001）。在血清中，sVEGFR-1 水平高于 PlGF（p <0.0001），而在血肿液中则不明显。此外，sVEGFR-1 与 PlGF 的比值在血肿液中明显低于血清（p <0.0001）。
鉴于先前的证据表明 PlGF 在促进血管生成、炎症细胞趋化和刺激以及在有利于病理性血管生成的条件下放大 VEGF 驱动的信号方面的作用，以及其在血肿液中增强表达的能力表明该因素参与了 CSDH 中的炎症和血管生成机制。此外，血肿液中 sVEGFR-1 与 PlGF 的比值降低与 CSDH 的促血管生成能力一致。需要进一步的研究来阐明 PlGF 和 sVEGFR-1 在 CSDH 中的确切作用。
