Caspase-3 and the regulation of hypoxic neuronal death by vascular endothelial growth factor

Jin, Kunlin; Mao, XiaoOu; Batteur, Sophie; McEachron, E; Leahy, Averi A.; Greenberg, David A.

doi:10.1016/s0306-4522(01)00154-3

Cited by 144 publications

(99 citation statements)

References 37 publications

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“…Given that VEGF is upregulated after seizures (Newton et al, 2003;Croll et al, 2004), it is possible that VEGF upregulation after seizures is an endogenous compensatory mechanism to reduce excitability. Indeed, after ischemia and traumatic brain injury, VEGF appears to be neuroprotective (Jin et al, 2000(Jin et al, , 2001. However, it is currently unclear whether the pharmacological studies of VEGF conducted to date, including the data presented here, reflect endogenous actions of VEGF.…”

Section: Discussionmentioning

confidence: 89%

“…VEGF enhances neuronal proliferation (Jin et al, 2002;Zhu et al, 2003), neurite outgrowth and maturation (Rosenstein et al, 2003;Khaibullina et al, 2004), and neuronal survival (Jin et al, 2000(Jin et al, , 2001Svensson et al, 2002). 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).…”

Section: Introductionmentioning

confidence: 99%

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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.

114

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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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Section: Discussionmentioning

confidence: 89%

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.

114

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show abstract

“…In endothelial cells, VEGF signaling through VEGFR2 promoted survival by preventing caspase-3 cleavage and p38 MAPK phosphorylation [25] while p38 MAPK inhibition enhanced ERK1/2 activation by VEGF [9]. In stressed neuronal cells, VEGF signals survival through its cognate receptor VEGFR2 and the downstream activation of the PI3K/Akt and MEK/ERK1/2 pathways [16,27] and by suppressing the activation of caspase-3 [10,16] and p38 MAPK [13]. However, the exact role of p38 MAPK in VEGF-mediated signaling under stressful conditions is unclear since VEGF was shown to stimulate p38 MAPK after brain hypoxia [9] and inhibit its activation after retinal ganglion cell axotomy [13].…”

Section: Introductionmentioning

confidence: 99%

p38 MAPK as a negative regulator of VEGF/VEGFR2 signaling pathway in serum deprived human SK-N-SH neuroblastoma cells

Gomes

Rockwell

2008

Neuroscience Letters

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Evidence suggests that vascular endothelial growth factor (VEGF) mediates neuroprotection to prevent an apoptotic cell death. The p38 mitogen activated protein kinase (MAPK) pathway is implicated as an important mediator of neuronal apoptosis but its role in VEGF-mediated neuroprotection is unclear. Herein, we show that treatments with the p38 MAPK inhibitor, SB202190, enhanced VEGF-mediated survival in serum deprived SK-N-SH neuroblastoma cells by decreasing caspase-3/7 activation while increasing the phosphorylation of the extracellular signalregulated kinase (ERK1/2) and Akt signaled through the VEGF receptor, VEGFR2. A blockade of VEGFR2 signaling with a selective inhibitor, SU1498 or gene silencing with VEGFR2 siRNA in SB202190 treated cells abrogated this prosurvival response and induced high activation levels of caspase-3/7. These findings suggested that the protection elicited by p38 MAPK inhibition in serum starved cells was dependent on a functional VEGF/VEGFR2 pathway. However, p38 MAPK inhibition attenuated caspase-3 cleavage in SU1498/SB202190 treated cells, indicating that p38 MAPK and caspase-3 only contributed in part to the total levels of caspase-3/7 induced by VEGFR2 inhibition. Pretreatments with the pan caspase inhibitor, z-VAD-fmk, prevented the apoptosis induced by VEGFR2 inhibition and promoted survival in serum starved cells irrespective of p38 MAPK inhibition. Collectively, our findings suggest that p38 MAPK exerts a negative effect on VEGF-mediated signaling through VEGFR2 in serum starved neuroblastoma cells. Furthermore, VEGF signals protection against a caspase-mediated cell death that is regulated by p38 MAPKdependent and -independent mechanisms.

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“…After activation through different pathways, caspase-8 and -9 can activate caspase-3. Activated caspase-3 can then induce cell apoptosis (Jin et al, 2001). In the process, proteins such as calpain, cathepsin and endonuclease perform programmed cell death and strengthen the apoptosis of cancer cells through interaction with caspases (Kajita et al, 2006).…”

Section: Gene Expression Of the Apoptosis-related Caspasesmentioning

confidence: 99%

Apoptotic effects of insect tea in HepG2 human hepatoma cells

Suo

Péng

Wang

et al. 2015

CyTA - Journal of Food

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Insect tea is a traditional and special tea in China. After the HepG2 cancer cells were treated with insect tea ethanol extracts (ITEE) for 48 h, HepG2 cell proliferation was inhibited, with 40, 80 and 160 μg/mL of ITEE showing inhibitory rates of 35.1%, 59.7% and 86.3%, respectively. Compared to the lower concentration, 160 μg/mL ITEE significantly induced apoptosis as determined by flow cytometry analysis, which showed the content of sub-G1 cancer cells was 38.8%. By RT-PCR, ITEE induced apoptosis in HepG2 cancer cells by increasing caspase-3, caspase-8, caspase-9, Bax, p53, p21, E2F1, p73 and decreasing Bcl-2, Bcl-xL, HIAP-1 and HIAP-2 mRNA expression levels. Insect tea is rich in polyphenols, caffeine, flavones, vitamin C and amino acids. There were 17 kinds of amino acids in insect tea. The functional components of insect tea induce apoptosis in HepG2 cancer cells. Insect tea is a good functional food by its anticancer effects.Keywords: insect tea; apoptosis; HepG2 cells; cancer; mRNA expression El té de insecto es un té tradicional y especial en China. Después que se trataran las células cancerígenas HepG2 con extractos de etanol del té de insecto (ITEE) durante 48 h, se inhibió la proliferación de las células HepG2 con 40, 80 y 160 μg/mL de ITEE mostrando unos niveles de inhibición de 35,1%, 59,7% y 86.3%, respectivamente. En comparación con una menor concentración, 160 μg/mL de ITEE indujo apoptosis de forma significativa como fue determinado mediante la citometría de flujo, la cual mostró que el contenido de células cancerígenas sub-G1 era de 38,8%. Mediante RT-PCR, el ITEE indujo apoptosis en las células cancerígenas HepG2 a través del aumento de caspasa-3, caspasa-8, caspasa-9, Bax, p53, p21, E2F1, p73 y disminuyendo los niveles de expresión de Bcl-2, Bcl-xL, HIAP-1 y HIAP-2 mRNA. El té de insecto es rico en polifenoles, cafeína, flavonas, vitamina C y aminoácidos. Se obtuvieron 17 tipos de aminoácidos en el té de insecto. Los componentes funcionales del té de insecto indujeron apoptosis en las células cancerígenas HepG2. El té de insecto se trata de una bebida funcional gracias a sus efectos anti cáncer.

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Caspase-3 and the regulation of hypoxic neuronal death by vascular endothelial growth factor

Cited by 144 publications

References 37 publications

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

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

p38 MAPK as a negative regulator of VEGF/VEGFR2 signaling pathway in serum deprived human SK-N-SH neuroblastoma cells

Apoptotic effects of insect tea in HepG2 human hepatoma cells

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