Microangiographic study of spinal cord injury and myelopathy

Shingu, H.; Kimura, Ikuo; Nasu, Y.; Shiotani, A.; Oh-hama, Mitsuru; Hijioka, Akihiko; Tanaka, J

doi:10.1038/sc.1989.27

Cited by 15 publications

(10 citation statements)

References 8 publications

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“…Tissue edema is one of the main causes of secondary damage after SCI (Shingu et al, 1989;Blight, 1991;Popovich et al, 1996;Tator & Koyanagi, 1997;Mautes et al, 2000;Bilgen et al, 2001;Westergren et al, 2001;Casella et al, 2002;Loy et al, 2002;Narayana et al, 2004;Maikos & Shreiber, 2007). Although application of VEGF after SCI increases vascular permeability and tissue edema in the spinal cord, deterioration of functional recovery has not been reported (Patel et al, 2009;Sundberg et al, 2010).…”

Section: Vegf-r1 Affects Vascular Permeability But Not Long-term Conmentioning

confidence: 99%

Distinct roles of endogenous vascular endothelial factor receptor 1 and 2 in neural protection after spinal cord injury

Shinozaki

Nakamura

Konomi

et al. 2014

Neuroscience Research

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Secondary degeneration after spinal cord injury (SCI) is caused by increased vascular permeability, infiltration of inflammatory cells, and subsequent focal edema. Therapeutic interventions using neurotrophic factors have focused on the prevention of such reactions to reduce cell death and promote tissue regeneration. Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. However, the effect of VEGF on SCI remains controversial. VEGF signaling is primarily regulated through two primary receptors, VEGF receptor 1 (VEGF-R1) and VEGF receptor 2 (VEGF-R2). The purpose of this study was to examine the effects of intraperitoneal administration of VEGF-R1- and VEGF-R2-neutralizing antibodies on a mouse model of SCI. VEGF-R1 blockade, but not VEGF-R2 blockade, decreased the permeability and infiltration of inflammatory cells, and VEGF-R2 blockade caused a significant increase in neuronal apoptosis in the acute phase of SCI. VEGF-R2 blockade decreased the residual tissue area and the number of neural fibers in the chronic phase of SCI. VEGF-R2 blockade worsened the functional recovery and prolonged the latency of motor evoked potentials. These data suggest that endogenous VEGF-R2 plays a crucial role in neuronal protection after SCI.

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Section: Vegf-r1 Affects Vascular Permeability But Not Long-term Conmentioning

confidence: 99%

Distinct roles of endogenous vascular endothelial factor receptor 1 and 2 in neural protection after spinal cord injury

Shinozaki

Nakamura

Konomi

et al. 2014

Neuroscience Research

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“…Regenerative attempts within the central nervous system (CNS) after trauma have been suggested to be limited by many factors, including the lack of an adequate blood supply (Goldsmith et al, 1985; de la Torre and Goldsmith, 1988, 1990; Shingu et al, 1989; Goldsmith, 1994; Zhang and Guth, 1997). However, increased vessel densities have been described at various intervals after SCI in cats (Means et al, 1978; Beggs and Waggener, 1979), guinea pigs (Blight, 1991), rats (Zhang and Guth, 1997; Imperato‐Kalmar et al, 1997), and humans (Shingu et al, 1989). Studies of BSB permeability dynamics by using quantitative autoradiography have suggested that the injured spinal cord vasculature actually remains in a state of active remodeling until at least 28 days postcontusive injury (Popovich et al, 1996).…”

mentioning

confidence: 99%

Temporal progression of angiogenesis and basal lamina deposition after contusive spinal cord injury in the adult rat

Loy

Crawford

Darnall

et al. 2002

J of Comparative Neurology

198

209

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After spinal cord injury (SCI), the absence of an adequate blood supply to injured tissues has been hypothesized to contribute to the lack of regeneration. In this study, blood vessel changes were examined in 28 adult female Fischer 344 rats at 1, 3, 7, 14, 28, and 60 days after a 12.5 g x cm NYU impactor injury at the T9 vertebral level. Laminin, collagen IV, endothelial barrier antigen (SMI71), and rat endothelial cell antigen (RECA-1) immunoreactivities were used to quantify blood vessel per area densities and diameters in ventral gray matter (VGM), ventral white matter (VWM), and dorsal columns (DC) at levels ranging 15 mm rostral and caudal to the epicenter. This study demonstrates an angiogenic response, defined as SMI71/RECA-1-immunopositive endothelial cells that colocalize with a robust deposition of basal lamina and basal lamina streamers, 7 days after injury within epicenter VGM. This angiogenesis diminishes concurrent with cystic cavity formation. GAP43- and neurofilament- (68 kDa and 210 kDa) immunopositive fiber outgrowth was associated with these new blood vessels by day 14. Between 28 and 60 days after injury, increases in SMI71-immunopositive blood vessel densities were observed in the remaining VWM and DC with a corresponding increase in vessel diameters up to 15 mm rostral and caudal to the epicenter. This second angiogenesis within VWM and DC, unlike the acute response observed in VGM, did not correspond to any previously described changes in locomotor behaviors in this model. We propose that therapies targeting angiogenic processes be directed at the interval between 3 and 7 days after SCI.

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“…It is therefore not surprising that major therapeutic efforts have been directed towards slowing down or reversing the progression of secondary events in SCI (Bradbury and McMahon, 2006;Rossignol et al, 2007). Dynamic vascular changes are thought to play an important role in the evolution of secondary injury in SCI (Shingu et al, 1989;Blight, 1991;Popovich et al, 1996;Tator and Koyanagi, 1997;Mautes et al, 2000;Westergren et al, 2001;Casella et al, 2002;Loy et al, 2002;Narayana et al, 2004;Maikos and Shreiber, 2007). Among others, some of the specific vascular changes include angiogenesis and disruption of the blood-spinal cord barrier (BSCB).…”

mentioning

confidence: 99%

Effect of VEGF Treatment on the Blood-Spinal Cord Barrier Permeability in Experimental Spinal Cord Injury: Dynamic Contrast-Enhanced Magnetic Resonance Imaging

Cohen¹,

Ahobila-Vajjula²,

Sundberg³

et al. 2009

Journal of Neurotrauma

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Compromised blood-spinal cord barrier (BSCB) is a factor in the outcome following traumatic spinal cord injury (SCI). Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis and vascular permeability. The role of VEGF in SCI is controversial. Relatively little is known about the spatial and temporal changes in the BSCB permeability following administration of VEGF in experimental SCI. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) studies were performed to noninvasively follow spatial and temporal changes in the BSCB permeability following acute administration of VEGF in experimental SCI over a post-injury period of 56 days. The DCE-MRI data was analyzed using a two-compartment pharmacokinetic model. Animals were assessed for open field locomotion using the Basso-Beattie-Bresnahan score. These studies demonstrate that the BSCB permeability was greater at all time points in the VEGF-treated animals compared to saline controls, most significantly in the epicenter region of injury. Although a significant temporal reduction in the BSCB permeability was observed in the VEGF-treated animals, BSCB permeability remained elevated even during the chronic phase. VEGF treatment resulted in earlier improvement in locomotor ability during the chronic phase of SCI. This study suggests a beneficial role of acutely administered VEGF in hastening neurobehavioral recovery after SCI.

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Microangiographic study of spinal cord injury and myelopathy

Cited by 15 publications

References 8 publications

Distinct roles of endogenous vascular endothelial factor receptor 1 and 2 in neural protection after spinal cord injury

Distinct roles of endogenous vascular endothelial factor receptor 1 and 2 in neural protection after spinal cord injury

Temporal progression of angiogenesis and basal lamina deposition after contusive spinal cord injury in the adult rat

Effect of VEGF Treatment on the Blood-Spinal Cord Barrier Permeability in Experimental Spinal Cord Injury: Dynamic Contrast-Enhanced Magnetic Resonance Imaging

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