Vascular endothelial growth factor signaling implicated in neuroprotective effects of placental growth factor in an in vitro ischemic model

Du, Huan; Li, Pengtao; Pan, Yanshu; Li, Weihong; Hou, Jincai; Chen, Huicong; Wang, Jun; Tang, Huiling

doi:10.1016/j.brainres.2010.07.015

Cited by 44 publications

(42 citation statements)

References 22 publications

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“…It is conceivable that PIGF may be upregulated after brain injuries. Indeed, recent studies showed that expression of PIGF was increased in the ischemic brain tissue [10,39]. In our study, the highest level of PIGF was seen in patients with secondary epilepsy while moderate level of PIGF presented in patients with idiopathic epilepsy.…”

Section: Discussioncontrasting

confidence: 40%

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

Zhang

Guo

et al. 2011

Neurochem Res

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Recent studies suggest that angiogenesis and vascular endothelial growth factor (VEGF) are involved in the pathophysiology of epilepsy. However, relatively little data are available linking placenta growth factor (PIGF) with epilepsy. In this study, we assessed concentrations of PIGF in cerebrospinal fluid (CSF) of 60 epileptic patients and 24 non-seizure subjects using sandwich enzyme-linked immunosorbent assays. Epileptic patients in general had higher concentration of CSF-PIGF than controls (7.95 ± 0.88 ng/l vs. 5.87 ± 0.79 ng/l, P < 0.01). CSF-PIGF level in secondary epileptic patients (8.59 ± 1.26 ng/l) was higher than that in idiopathic epileptic patients (7.62 ± 0.20 ng/l) (P < 0.05). In idiopathic epilepsy, CSF-PIGF level in patients with high seizure frequency was higher than those in patients with low seizure frequency and seizure-free in recent 3 years (7.78 ± 0.23 ng/l vs. 7.49 ± 0.09 ng/l and 7.59 ± 0.10 ng/l, P < 0.05). Concentration of CSF-PIGF in patients with a disease duration of > 5 years was higher than those in patients with durations of 1-5 years and <1 year (7.72 ± 0.20 ng/l vs. 7.52 ± 0.09 ng/l and 7.41 ± 0.07 ng/l, P < 0.05). These results indicate that preexisting brain damage, seizure frequency and disease duration are important factors contributing to elevated PIGF.

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Section: Discussioncontrasting

confidence: 40%

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

Zhang

Guo

et al. 2011

Neurochem Res

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“…It also promotes survival of cortical neurons (Du et al 2010), promotes axon growth cone formation of dorsal root ganglion neurons , and stimulates proliferation and migration of Schwann cells (Chaballe et al 2011a). PlGF enhances growth of tumor cells, both of solid and hematological tumors (Fischer et al 2008;Schmidt et al 2011).…”

Section: Plgf: a Pleiotropic Factormentioning

confidence: 99%

“…Intravenous delivery of PlGF-overexpressing mesenchymal stem cells (MSCs) to rats with surgically induced cerebral ischemia reduces lesion size, increases angiogenesis, and attenuates ischemia-induced functional deficits (Liu et al 2006). PlGF also promotes the survival of cortical neurons in vitro under oxygen and glucose deprivation (Du et al 2010). On the other side, PlGF deficiency renders astrocytes more resistant to oxygen and glucose deprivation in vitro (Freitas-Andrade et al 2008).…”

Section: Nervous Systemmentioning

confidence: 99%

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

Dewerchin¹,

Carmeliet²

2012

Cold Spring Harbor Perspectives in Medicine

187

172

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“…BECs can produce some of these cytokines (such as VEGF and BDNF) and participate in the regulation of neuronal activity (Wang et al 2006). In previously published studies, we found paracrine signaling of brain microvascular endothelial cells plays important roles in the survival of neurons under normal conditions and following injury (Du et al 2010;Li et al 2009). In this study, we isolated and cultured mouse BECs (Fig.…”

Section: Discussionmentioning

confidence: 92%

“…Western blot analysis was performed as described previously (Du et al 2010). Total lysate from cultured cells was used for detection of MMP-2 and cell signaling expression.…”

Section: Western Blot Analysismentioning

confidence: 99%

The Interaction of Amyloid β and the Receptor for Advanced Glycation Endproducts Induces Matrix Metalloproteinase-2 Expression in Brain Endothelial Cells

Du,

Li,

Wang

et al. 2011

Cell Mol Neurobiol

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The pathological hallmarks of Alzheimer's disease (AD) include formation of extracellular amyloid-β peptide (Aβ) and inflammatory responses. Numerous studies have reported that cerebral microvascular Aβ deposition promotes neuroinflammation in AD. Matrix metalloproteinases (MMPs) are involved in the cleavage of extracellular matrix proteins and regulation of growth factors, receptors, and adhesion molecules. Relatively little is known about the involvement of MMPs as inflammatory mediators in the pathological processes of AD. In this study, we explored the signaling pathway of MMP-2 up-regulation by Aβ in brain endothelial cells (BECs) of mice. Using Western blots, we found that inhibitors of extracellular-signal-regulated kinases (ERK) and c-Jun N-terminal kinase (JNK) significantly decreased Aβ-induced MMP-2 expression in BECs. Furthermore, antibody neutralization of the receptor for advanced glycation endproducts effectively blocked Aβ-induced activation of ERK and JNK and their contribution to elevated MMP-2 expression in BECs. Our results suggest that increased MMP-2 expression induced by the interaction of Aβ with RAGE in BECs may contribute to enhanced vascular inflammatory stress in Aβ-related vascular disorders, such as cerebral amyloid angiopathy and AD. This study offers new insights into neuroinflammation in the progression of AD.

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Vascular endothelial growth factor signaling implicated in neuroprotective effects of placental growth factor in an in vitro ischemic model

Cited by 44 publications

References 22 publications

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

The Interaction of Amyloid β and the Receptor for Advanced Glycation Endproducts Induces Matrix Metalloproteinase-2 Expression in Brain Endothelial Cells

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