Vascular endothelial growth factor

Neurosurgery 77:274–282, 2015

Biochemical alterations associated with mechanical stress have been explored as an initiating step in the pathological progression of ligamentum flavum hypertrophy (LFH); however, this mechanism remains poorly understood. Recently, the inflammation induced after mechanical stress and the subsequent response of ligamentum flavum (LF) cells have been implicated in LFH pathology.

OBJECTIVE: To investigate the hypothesis that angiogenesis may be a critical link between hypertrophy and a series of stimulating events, including mechanical stress.

METHODS: LF from 20 lumbar spinal canal stenosis (LSCS) patients and 16 non-LSCS patients (control group) were collected during surgery. Patient demographic and radiographic data were obtained. The levels of angiogenic factors (vascular endothelial growth factor [VEGF], angiopoietin-1, vascular cell adhesion molecule, and basic fibroblast growth factor) in the LF were investigated by using an enzyme-linked immunosorbent assay. Angiogenesis was also quantified by immunohistochemical detection of CD34-positive capillaries. The correlations among clinical factors, including radiographic factors, angiogenic factors, and angiogenesis, were statistically analyzed.

RESULTS: The LSCS group was older and exhibited a longer symptom duration, wider segmental motion, and thicker LF than the control group. The LSCS group showed significantly higher tissue concentrations of VEGF (P , .001) that positively correlated with LF thickness (r = 0.557, P , .001) and segmental motion (r = 0.586, P , .001). The LSCS group showed significantly more CD34-positive capillaries than the control group (P = .004).

CONCLUSION: The LSCS group showed greater segmental motion, higher VEGF concentrations, and more CD34-positive capillaries than the control group. These data indicate that VEGF-mediated angiogenesis following mechanical stress may be a critical step within the series of pathological events in LFH.

Neurosurgery 67:1703–1708, 2010 DOI: 10.1227/NEU.0b013e3181fb801b

Peritumoral brain edema (PTBE) may be crucial in the clinical outcome of meningioma patients. The underlying pathogenetic key mechanism has so far not been determined. Sex, age, tumor size, location, involvement of other structures, or the histological appearance was not found to sufficiently explain PTBE formation in meningiomas.

OBJECTIVE: As PTBE formation is widely accepted to be vasogenic, we investigated the role of vascular endothelial growth factor (VEGF) and pial supplying vessels in a series of World Health Organization (WHO) grade I meningiomas.

METHODS: A total of 79 patients with WHO grade I meningiomas were immunohistochemically studied for VEGF and MIB-1. Pre- and postoperative magnetic resonance imaging including 3-dimensional reconstruction of 1.3-mm thick layers, with calculation of tumor and edema volume, was performed. Intraoperatively, the vascular supply and arachnoidal state were noted by the neurosurgeon.

RESULTS: VEGF was found to be exclusively confined to meningioma tumor cells. We identified 4 different patterns. VEGF and supplying pial vessels were found in 14 meningioma patients, pial vascular supply only in 3, VEGF expression only in 46, and neither VEGF expression nor supplying pial vessels in 16. Only the occurrence of both pial vascular supply and tumor VEGF expression was found to be correlated with PTBE formation (P , .002).

CONCLUSION: Our data suggest that VEGF may be crucial in angiogenesis and therefore indirectly in PTBE formation in World Health Organization grade I meningiomas

Tag: Vascular endothelial growth factor

The Mechanism of Ligamentum Flavum Hypertrophy

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