New Vascular Tissue Rapidly Replaces Neural Parenchyma and Vessels Destroyed by a Contusion Injury to the Rat Spinal Cord

Casella, Gizelda; Marcillo, Alexander; Bunge, Mary Bartlett; Wood, Patrick M.

doi:10.1006/exnr.2001.7827

Cited by 143 publications

(132 citation statements)

References 42 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…6E,F,H,I), revealing multiple pathological aspects of the intrinsic neoangiogenesis, consistent with previous reports. 11,42,[48][49][50] During these two weeks, ChABC treatment did not appear to modify the density or the labeling of RECA-1 positive blood vessels (Fig. 6).…”

Section: Intrathecal Chabc Injections Induce Cspg Degradation At the mentioning

confidence: 84%

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Milbreta

Boxberg

Mailly

et al. 2014

Journal of Neurotrauma

View full text Add to dashboard Cite

Upregulation of extracellular chondroitin sulfate proteoglycans (CSPG) is a primary cause for the failure of axons to regenerate after spinal cord injury (SCI), and the beneficial effect of their degradation by chondroitinase ABC (ChABC) is widely documented. Little is known, however, about the effect of ChABC treatment on astrogliosis and revascularization, two important factors influencing axon regrowth. This was investigated in the present study. Immediately after a spinal cord hemisection at thoracic level 8-9, we injected ChABC intrathecally at the sacral level, repeated three times until 10 days post-injury. Our results show an effective cleavage of CSPG glycosaminoglycan chains and stimulation of axonal remodeling within the injury site, accompanied by an extended period of astrocyte remodeling (up to 4 weeks). Interestingly, ChABC treatment favored an orientation of astrocytic processes directed toward the injury, in close association with axons at the lesion entry zone, suggesting a correlation between axon and astrocyte remodeling. Further, during the first weeks post-injury, ChABC treatment affected the morphology of laminin-positive blood vessel basement membranes and vessel-independent laminin deposits: hypertrophied blood vessels with detached or duplicated basement membrane were more numerous than in lesioned untreated animals. In contrast, at later time points, laminin expression increased and became more directly associated with newly formed blood vessels, the size of which tended to be closer to that found in intact tissue. Our data reinforce the idea that ChABC injection in combination with other synergistic treatments is a promising therapeutic strategy for SCI repair.

show abstract

Section: Intrathecal Chabc Injections Induce Cspg Degradation At the mentioning

confidence: 84%

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Milbreta

Boxberg

Mailly

et al. 2014

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…This summarizes data from several studies that have addressed the timing of infiltration relative to early injury and wound healing events. Peak periods of infiltration coincide with barrier disruption (91,92) , angiogenesis (93)(94)(95) , and glial scar formation (11) . Note that the magnitude of infiltration is expressed as arbitrary units for each of the cell types, and as such comparisons cannot be made between groups.…”

Section: Resultsmentioning

confidence: 99%

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

195

138

View full text Add to dashboard Cite

The immune response that accompanies spinal cord injury contributes to both injury and reparative processes. It is this duality that is the focus of this review. Here we consider the complex cellular and molecular immune responses that lead to the infiltration of leukocytes and glial activation, promote oxidative stress and tissue damage, influence wound healing, and subsequently modulate locomotor recovery. Immunomodulatory strategies to improve outcomes are gaining momentum as ongoing research carefully dissects those pathways, which likely mediate cell injury from those, which favor recovery processes. Current therapeutic strategies address divergent approaches including early immunoblockade and vaccination with immune cells to prevent early tissue damage and support a wound-healing environment that favors plasticity. Despite these advances, there remain basic questions regarding how inflammatory cells interact in the injured spinal cord. Such questions likely arise as a result of our limited understanding of immune cell/neural interactions in a dynamic environment that culminates in progressive cell injury, demyelination, and regenerative failure.

show abstract

“…Sections stained for BrdU were pretreated with 2N HCl for 30 min and neutralized with sodium borate buffer, pH 8.4, before incubation in primary antibody (Tsai et al, 2006). Sections stained for laminin were pretreated by boiling in distilled water (Casella et al, 2002).…”

Section: Methodsmentioning

confidence: 99%

A Neurovascular Niche for Neurogenesis after Stroke

Ohab¹,

Fleming²,

Blesch³

et al. 2006

J. Neurosci.

798

783

View full text Add to dashboard Cite

Stroke causes cell death but also birth and migration of new neurons within sites of ischemic damage. The cellular environment that induces neuronal regeneration and migration after stroke has not been defined. We have used a model of long-distance migration of newly born neurons from the subventricular zone to cortex after stroke to define the cellular cues that induce neuronal regeneration after CNS injury. Mitotic, genetic, and viral labeling and chemokine/growth factor gain-and loss-of-function studies show that stroke induces neurogenesis from a GFAP-expressing progenitor cell in the subventricular zone and migration of newly born neurons into a unique neurovascular niche in peri-infarct cortex. Within this neurovascular niche, newly born, immature neurons closely associate with the remodeling vasculature. Neurogenesis and angiogenesis are causally linked through vascular production of stromal-derived factor 1 (SDF1) and angiopoietin 1 (Ang1). Furthermore, SDF1 and Ang1 promote post-stroke neuroblast migration and behavioral recovery. These experiments define a novel brain environment for neuronal regeneration after stroke and identify molecular mechanisms that are shared between angiogenesis and neurogenesis during functional recovery from brain injury.

show abstract

New Vascular Tissue Rapidly Replaces Neural Parenchyma and Vessels Destroyed by a Contusion Injury to the Rat Spinal Cord

Cited by 143 publications

References 42 publications

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

A Neurovascular Niche for Neurogenesis after Stroke

Contact Info

Product

Resources

About