Vascular endothelial growth factor improves functional outcome and decreases secondary degeneration in experimental spinal cord contusion injury

Widenfalk, Johan; Lipson, Adam C.; Jubran, Marie; Hofstetter, Christoph P.; Ebendal, Ted; Cao, Yihai; Olson, Lar̀s

doi:10.1016/s0306-4522(03)00399-3

Cited by 222 publications

(198 citation statements)

References 55 publications

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“…We have no data to support the idea that there is cortical neurogenesis in the visual cortex due to the infusion of VEGF, as occurs in vitro or in other regions (Palmer et al, 2000;Louissaint et al, 2002;Maurer et al, 2003;Rosenstein et al, 2003;Sun et al, 2003). Previous studies have reported that the administration of VEGF reduces the increase of apoptosis in experimental spinal cord injury (Widenfalk et al, 2003). In agreement with them, we also suggest that VEGF infusion rescues neurons from physiological apoptosis.…”

Section: Neuronal Densitycontrasting

confidence: 40%

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

et al. 2012

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Section: Neuronal Densitycontrasting

confidence: 40%

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

et al. 2012

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“…On the other hand, while VEGF was originally discovered as an angiogenic factor, recent studies have indicated that it also has direct neurotrophic effects on the central and peripheral nervous systems. VEGF stimulates axonal outgrowth and enhances the survival of superior cervical and DRG neurons [21,22], promotes neurogenesis in vitro and in vivo [7], and improves neuronal function and decreases degeneration after experimental spinal cord injury [26]. Another study suggested that endogenous VEGF has effects on neurons [12].…”

Section: Discussionmentioning

confidence: 99%

Spinal stenosis: assessment of motor function, VEGF expression and angiogenesis in an experimental model in the rat

et al. 2007

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Reduction of blood flow in compressed nerve roots is considered as one important mechanism of induction of neurogenic intermittent claudication in lumbar spinal canal stenosis. Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis, and is increased in expression in hypoxic conditions. The objective of this study was to examine if cauda equina compression affects motor function and induces expression of VEGF and angiogenesis. The cauda equina was compressed by placing a piece of silicone rubber into the L5 epidural space. Walking duration was examined by rota-rod testing. The compressed parts of the cauda equina and L5 dorsal root ganglion (DRG) were removed at 3, 7, 14, or 28 days after surgery, and processed for immunohistochemistry for VEGF and Factor VIII (marker for vascular endothelial cells). Numbers of VEGF-immunoreactive (IR) cells and vascular density were examined. Walking duration was decreased after induction of cauda equina compression. The number of VEGF-IR cells in the cauda equina and DRG was significantly increased at 3, 14, and 28 days after cauda equina compression, compared with sham-operated rats (P < 0.05). Vascular density in the cauda equina was not increased at any of the time points examined. Cauda equina compression decreased walking duration, and induced VEGF expression in nerve roots and DRG.

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“…40 Numerous reports have suggested that stimulation of post-traumatic angiogenesis with angiogenic factors such as VEGF promotes neuroregeneration and improves functional recovery after SCI. 41,42 Optimizing treatments to target vascularization after SCI is a valuable therapeutic strategy.…”

Section: The Clinical Applications Of Mtor Inhibitorsmentioning

confidence: 99%

The role of mTOR signaling pathway in spinal cord injury

et al. 2012

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T he mammalian target of rapamycin (mTOR) signaling pathway plays an important role in multiple cellular functions, such as cell metabolism, proliferation and survival. Many previous studies have shown that mTOR regulates both neuroprotective and neuroregenerative functions in trauma and various diseases in the central nervous system (CNS). Recently, we reported that inhibition of mTOR using rapamycin reduces neural tissue damage and locomotor impairment after spinal cord injury (SCI) in mice. Our results demonstrated that the administration of rapamycin at four hours after injury significantly increases the activity of autophagy and reduces neuronal loss and cell death in the injured spinal cord. Furthermore, rapamycintreated mice show significantly better locomotor function in the hindlimbs following SCI than vehicle-treated mice. These findings indicate that the inhibition of mTOR signaling using rapamycin during the acute phase of SCI produces neuroprotective effects and reduces secondary damage at lesion sites. However, the role of mTOR signaling in injured spinal cords has not yet been fully elucidated. Various functions are regulated by mTOR signaling in the CNS, and multiple pathophysiological processes occur following SCI. Here, we discuss several unresolved issues and review the evidence from related articles regarding the role and mechanisms of the mTOR signaling pathway in neuroprotection and neuroregeneration after SCI.

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Vascular endothelial growth factor improves functional outcome and decreases secondary degeneration in experimental spinal cord contusion injury

Cited by 222 publications

References 55 publications

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

Spinal stenosis: assessment of motor function, VEGF expression and angiogenesis in an experimental model in the rat

The role of mTOR signaling pathway in spinal cord injury

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