Early neutrophilic expression of vascular endothelial growth factor after traumatic brain injury

Chodobski, Adam; Chung, In-Sung; Koźniewska, Ewa; Ivanenko, T; Chang, Wen-I; Harrington, J. Frederick; Duncan, John A.; Szmydynger‐Chodobska, Joanna

doi:10.1016/j.neuroscience.2003.08.055

Cited by 80 publications

(66 citation statements)

References 55 publications

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“…Recent studies have demonstrated PMN and neutrophils in particular to express VEGF. 11,12 Thus, the elevated local VEGF in wound fluids during VAC™ therapy in our study can be explained by increased and early accumulation of neutrophils as shown histologically. Elevated levels of VEGF were also demonstrated in our previous investigation where cytokines were measured in wound fluids of patients with traumatic wounds treated initially with Epigard followed by VAC therapy.…”

Section: Discussionsupporting

confidence: 52%

“…10 PMN have recently been shown to express vascular endothelial growth factor (VEGF), and following traumatic brain injury, an early increase in VEGF expression was described within 4 hours post-injury in the traumatized parenchyma associated with invasion of neutrophils granulocytes. 11,12 VEGF is a growth factor which promotes neovascularization through extension and growth of existing arterial and capillary networks. 13 Macrophages, in addition, infiltrating the wound after PMN, modulate the wound angiogenesis by releasing angiogenic factors such as fibroblast growth factor (FGF)-2 and VEGF.…”

Section: A and B)mentioning

confidence: 99%

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Vacuum-Assisted Closure Therapy Increases Local Interleukin-8 and Vascular Endothelial Growth Factor Levels in Traumatic Wounds

Labler

Rancan

Mica

et al. 2009

Journal of Trauma: Injury, Infection &Amp; Critical Care

148

116

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BACKGROUND: Clinical observations are suggesting accelerated granulation tissue formation in traumatic wounds treated with vacuum-assisted closure (VAC). Aim of this study was to determine the impact of VAC therapy versus alternative Epigard application on local inflammation and neovascularization in traumatic soft tissue wounds. METHODS: Thirty-two patients with traumatic wounds requiring temporary coverage (VAC n = 16; Epigard n = 16) were included. At each change of dressing, samples of wound fluid and serum were collected (n = 80). The cytokines interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), and fibroblast growth factor-2 were measured by ELISA. Wound biopsies were examined histologically for inflammatory cells and degree of neovascularization present. RESULTS: All cytokines were found to be elevated in wound fluids during both VAC and Epigard treatment, whereas serum concentrations were negligible or not detectable. In wound fluids, significantly higher IL-8 (p < 0.001) and VEGF (p < 0.05) levels were detected during VAC therapy. Furthermore, histologic examination revealed increased neovascularization (p < 0.05) illustrated by CD31 and von Willebrand factor immunohistochemistry in wound biopsies of VAC treatment. In addition, there was an accumulation of neutrophils as well as an augmented expression of VEGF (p < 0.005) in VAC wound biopsies. CONCLUSION: This study suggests that VAC therapy of traumatic wounds leads to increased local IL-8 and VEGF concentrations, which may trigger accumulation of neutrophils and angiogenesis and thus, accelerate neovascularization.

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Section: Discussionsupporting

confidence: 52%

Section: A and B)mentioning

confidence: 99%

Vacuum-Assisted Closure Therapy Increases Local Interleukin-8 and Vascular Endothelial Growth Factor Levels in Traumatic Wounds

Labler

Rancan

Mica

et al. 2009

Journal of Trauma: Injury, Infection &Amp; Critical Care

148

116

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“…TGFb1 is an important cytokine that is rapidly induced following TBI (Wang et al, 2007). It has many functions in the nervous system, which are both beneficial and detrimental to the recovery from TBI including promoting glial scar formation (Chodobski et al, 2003;Vivien and Ali, 2006;Wang et al, 2007). Ang II can induce the expression or activation of TGFb1 in many different tissues (Harasawa et al, 2010;Jiao et al, 2011;Sun et al, 1998;Yu et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Candesartan, an Angiotensin II AT1-Receptor Blocker and PPAR-γ Agonist, Reduces Lesion Volume and Improves Motor and Memory Function After Traumatic Brain Injury in Mice

Villapol

Yaszemski

Logan

et al. 2012

Neuropsychopharmacol

103

107

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Traumatic brain injury (TBI) results in complex pathological reactions, the initial lesion worsened by secondary inflammation and edema. Angiotensin II (Ang II) is produced in the brain and Ang II receptor type 1 (AT 1 R) overstimulation produces vasoconstriction and inflammation. Ang II receptor blockers (ARBs) are neuroprotective in models of stroke but little is known of their effect when administered in TBI models. We therefore performed controlled cortical impact (CCI) injury on mice to investigate whether the ARB candesartan would mitigate any effects of TBI. We administered candesartan or vehicle to mice 5 h before CCI injury. Candesartan treatment reduced the lesion volume after CCI injury by approximately 50%, decreased the number of dying neurons, lessened the number of activated microglial cells, protected cerebral blood flow (CBF), and reduced the expression of the cytokine TGFb1 while increasing expression of TGFb3. Candesartan-treated mice also showed better motor skills on the rotarod 3 days after injury, and improved performance in the Morris water maze 4 weeks after injury. These results indicate that candesartan is neuroprotective, reducing neuronal injury, decreasing lesion volume and microglial activation, protecting CBF and improving functional behavior in a mouse model of TBI. Co-treatment with a peroxisome proliferator-activated receptor-gamma (PPARg) antagonist significantly reduced some of the beneficial effects of candesartan after CCI, suggesting that PPARg activation may contribute to part or to all of the neuroprotective effect of candesartan. Overall, our data suggest that ARBs with dual AT 1 R-blocking and PPARg activation properties may have therapeutic value in treating TBI.

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“…A neuroprotective role for VEGF is supported by the demonstration that VEGF reduces excitotoxic damage to cultured hippocampal neurons (Jin et al, 2000;Matsuzaki et al, 2001;Svensson et al, 2002) and reduces damage in vivo after ischemia (Hayashi et al, 1998;Sun et al, 2003) (but see van Bruggen et al, 1999). Together with the evidence that VEGF expression increases after ischemia , traumatic brain injury (Chodobski et al, 2003), and seizures (Newton et al, 2003;Croll et al, 2004), it is possible that VEGF is an endogenous neuroprotective agent in the CNS. However, despite the potential importance of VEGF as a neuroprotective growth factor, few direct studies of VEGF on neurons or glia have been published to clarify its actions.…”

Section: Introductionmentioning

confidence: 99%

Depression of Synaptic Transmission by Vascular Endothelial Growth Factor in Adult Rat Hippocampus and Evidence for Increased Efficacy after Chronic Seizures

McCloskey¹,

Croll²,

Scharfman³

2005

J. Neurosci.

115

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In addition to its potent effects on vasculature, it has become clear that vascular endothelial growth factor (VEGF) has effects on both neurons and glia, and recent studies suggest that it can be neuroprotective. To determine potential mechanisms underlying this neuroprotection, recombinant human VEGF was bath applied to adult rat hippocampal slices, and both extracellular and intracellular recordings were used to examine intrinsic properties and synaptic responses of hippocampal principal neurons. Initial studies in area CA1 showed that VEGF significantly reduced the amplitude of responses elicited by Schaffer collateral stimulation, without influencing membrane properties. Similar effects occurred in CA3 pyramidal cells and dentate gyrus granule cells when their major glutamatergic afferents were stimulated. Because VEGF expression is increased after seizures, effects of VEGF were also examined in rats with recurrent spontaneous seizures. VEGF reduced spontaneous discharges in slices from these rats but had surprisingly little effect on epileptiform discharges produced by disinhibition of slices from control rats. These results demonstrate a previously unknown effect of VEGF on neuronal activity and also demonstrate a remarkable potency in the epileptic brain. Based on this, we suggest that VEGF or VEGF-related targets could provide useful endpoints to direct novel therapeutic strategies for epilepsy.

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Early neutrophilic expression of vascular endothelial growth factor after traumatic brain injury

Cited by 80 publications

References 55 publications

Vacuum-Assisted Closure Therapy Increases Local Interleukin-8 and Vascular Endothelial Growth Factor Levels in Traumatic Wounds

Vacuum-Assisted Closure Therapy Increases Local Interleukin-8 and Vascular Endothelial Growth Factor Levels in Traumatic Wounds

Candesartan, an Angiotensin II AT1-Receptor Blocker and PPAR-γ Agonist, Reduces Lesion Volume and Improves Motor and Memory Function After Traumatic Brain Injury in Mice

Depression of Synaptic Transmission by Vascular Endothelial Growth Factor in Adult Rat Hippocampus and Evidence for Increased Efficacy after Chronic Seizures

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