Phospholipase C, protein kinase C, Ca<sup>2+</sup>/calmodulin‐dependent protein kinase II, and redox state are involved in epigallocatechin gallate‐induced phospholipase D activation in human astroglioma cells

Kim, Shi Yeon; Ahn, Bong-Hyun; Kim, Joonmo; Bae, Yoe‐Sik; Kwak, Jong‐Young; Min, Gyesik; Kwon, Taeg Kyu; Chang, Jong-Soo; Lee, Young Han; Yoon, Sung Hyun; Min, Do Sik

doi:10.1111/j.0014-2956.2004.04242.x

Cited by 26 publications

(23 citation statements)

References 41 publications

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“…PKC ␣ is a well-established neuron cell survival factor participating also in cell growth and differentiation [63,64] . In support, a recent report shows that treatment of human cells with EGCG induces a specifi c translocation of PKC ␣ to the membrane [65] .…”

Section: Mechanism Of Neuroprotection By Green Tea Catechinssupporting

confidence: 62%

Multifunctional Activities of Green Tea Catechins in Neuroprotection

Mandel¹,

Avramovich-Tirosh²,

Reznichenko³

et al. 2005

Neurosignals

312

111

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Many lines of evidence suggest that oxidative stress resulting in reactive oxygen species (ROS) generation and inflammation play a pivotal role in the age-associated cognitive decline and neuronal loss in neurodegenerative diseases including Alzheimer’s (AD), Parkinson’s (PD) and Huntington’s diseases. One cardinal chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. The buildup of an iron gradient in conjunction with ROS (superoxide, hydroxyl radical and nitric oxide) are thought to constitute a major trigger in neuronal toxicity and demise in all these diseases. Thus, promising future treatment of neurodegenerative diseases and aging depends on availability of effective brain permeable, iron-chelatable/radical scavenger neuroprotective drugs that would prevent the progression of neurodegeneration. Tea flavonoids (catechins) have been reported to possess potent iron- chelating, radical-scavenging and anti-inflammatory activities and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. Recent studies have indicated that in addition to the known antioxidant activity of catechins, other mechanisms such as modulation of signal transduction pathways, cell survival/death genes and mitochondrial function, contribute significantly to the induction of cell viability. This review will focus on the multifunctional properties of green tea and its major component (–)-epigallocatechin-3-gallate (EGCG) and their ability to induce neuroprotection and neurorescue in vitro and in vivo. In particular, their transitional metal (iron and copper) chelating property and inhibition of oxidative stress.

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Section: Mechanism Of Neuroprotection By Green Tea Catechinssupporting

confidence: 62%

Multifunctional Activities of Green Tea Catechins in Neuroprotection

Mandel¹,

Avramovich-Tirosh²,

Reznichenko³

et al. 2005

Neurosignals

312

111

View full text Add to dashboard Cite

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“…Several studies suggest that PLC␥1 regulates PLD activity in intracellular signal transduction (42,53,54). Thus, we tried to determine whether PLC␥ signaling pathway is involved in Der f 2-induced PLD activation and found that pretreatment with U73122 or PAO, specific PLC␥ inhibitors, completely blocked Der f 2-induced PLD1 activation and IL-13 production in BEAS-2B cells, suggesting that PLC␥ activation is related to PLD activation and IL-13 production.…”

Section: Discussionmentioning

confidence: 99%

“…To investigate how Der f 2 activates PLD1, we examined PLC␥ signaling because there are studies suggesting that PLC␥ activation results in increased PLD activity (42). The mammalian PLC␥ family has two closely related members, PLC␥1 and PLC␥2.…”

Section: Der F 2-induced Il-13 Production and Expression Are Regulatementioning

confidence: 99%

House Dust Mite Allergen Der f 2-induced Phospholipase D1 Activation Is Critical for the Production of Interleukin-13 through Activating Transcription Factor-2 Activation in Human Bronchial Epithelial Cells

Park

Cho

et al. 2009

Journal of Biological Chemistry

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The purpose of this study was to identify the role of phospholipase D1 (PLD1) in Der f 2-induced interleukin (IL)-13 production. The major house dust mite allergen, Der f 2, increased PLD activity in human bronchial epithelial cells (BEAS-2B), and dominant negative PLD1 or PLD1 siRNA decreased Der f 2-induced IL-13 expression and production. Treatment of Der f 2 activated the phospholipase C␥ (PLC␥)/protein kinase C␣ (PKC␣)/p38 MAPK pathway. Der f 2-induced PLD activation was attenuated by PLC␥ inhibitors (U73122 and PAO), PKC␣ inhibitors (RO320432 and GO6976), and p38 MAPK inhibitors (SB203580 and SB202190). These results indicate that PLC␥, PKC␣, and p38 MAPK act as upstream activators of PLD in Der f 2-treated BEAS-2B cells. Furthermore, expression and production of IL-13 increased by Der f 2 were also blocked by inhibition of PLC␥, PKC␣, or p38 MAPK, indicating that IL-13 expression and production are related to a PLC␥/PKC␣/p38 MAPK pathway. We found that activating transcription factor-2 (ATF-2) was activated by Der f 2 in BEAS-2B cells and activation of ATF-2 was controlled by PLD1. When ATF-2 activity was blocked with ATF-2 siRNA, Der f 2-induced IL-13 expression and production were decreased. Thus, ATF-2 might be one of the transcriptional factors for the expression of IL-13 in Der f 2-treated BEAS-2B cells. Taken together, PLD1 acts as an important regulator in Der f 2-induced expression and production of IL-13 through activation of ATF-2 in BEAS-2B cells.

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“…It has been found that PI-PLC activation results in the generation of diacylglycerol (DAG) and inositol 1, 4, 5-triphosphate which activates protein kinase C (PKC) and mobilizes Ca 2þ , respectively [Kim et al, 2004]. We have already demonstrated that PKC is not involved in hippocalcin-induced PLD2 expression pathway.…”

Section: Discussionmentioning

confidence: 99%

“…There have been a few reports suggesting that some of the intracellular LPA actions require the PLD signaling via protein kinase C (PKC) [Gustavsson et al, 1994;Kim et al, 2004]. To determine whether PKC is involved in hippocalcin-induced PLD2 expression potentiated by LPA, we examined the effect of PKC downregulation on hippocalcin-induced PLD2 expression potentiated by LPA.…”

Section: Pkc Is Not Involved In the Hippocalcin-induced Pld2 Expressionmentioning

confidence: 99%

Hippocalcin increases phospholipase D2 expression through extracellular signal‐regulated kinase activation and lysophosphatidic acid potentiates the hippocalcin‐induced phospholipase D2 expression

Yon

et al. 2005

J of Cellular Biochemistry

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We have previously isolated a 22 kDa protein from a rat brain which was found to be involved in activating phospholipsae D (PLD), and identified the protein as hippocalcin through sequence analysis. Nevertheless, the function of hippocalcin for PLD activation still remains to be resolved. Here, we proposed that hippocalcin was involved in extracellular signal-regulated kinase (ERK)-mediated PLD2 expression. To elucidate a role of hippocalcin, we made hippocalcin transfected NIH3T3 cells and showed that the expression of PLD2 and basal PLD activity were increased in hippocalcin transfected cells. We performed PLD assay with dominant negative PLD2 (DN-PLD2) and hippocalcin co-transfected cells. DN-PLD2 suppressed increase of basal PLD activity in hippocalcin transfected cells, suggesting that increased basal PLD activity is due to PLD2 over-expression. Hippocalcin is a Ca2+-binding protein, which is expressed mainly in the hippocampus. Since it is known that lysophosphatidic acid (LPA) increases intracellular Ca2+, we investigated the possible role of hippocalcin in the LPA-induced elevation of intracellular Ca2+. When the intracellular Ca2+ level was increased by LPA, hippocalcin was translocated to the membrane after LPA treatment in hippocalcin transfected cells. In addition, treatment with LPA in hippocalcin transfected cells markedly potentiated PLD2 expression and showed morphological changes of cell shape suggesting that increased PLD2 expression acts as one of the major factors to cause change of cell shape by making altered membrane lipid composition. Hippocalcin-induced PLD2 expression potentiated by LPA in hippocalcin transfected cells was inhibited by a PI-PLC inhibitor, U73122 and a chelator of intracellular Ca2+, BAPTA-AM suggesting that activation of hippocalcin caused by increased intracellular Ca2+ is important to induce over-expression of PLD2. However, downregulation of PKC and treatment of a chelator of extracellular Ca2+, EGTA had little or no effect on the inhibition of hippocalcin-induced PLD2 expression potentiated by LPA in the hippocalcin transfected cells. Interestingly, when we over-express hippocalcin, ERK was activated, and treatment with LPA in hippocalcin transfected cells significantly potentiated ERK activation. Specific inhibition of ERK dramatically abolished hippocalcin-induced PLD2 expression. Taken together, these results suggest for the first time that hippocalcin can induce PLD2 expression and LPA potentiates hippocalcin-induced PLD2 expression, which is mediated by ERK activation.

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Phospholipase C, protein kinase C, Ca²⁺/calmodulin‐dependent protein kinase II, and redox state are involved in epigallocatechin gallate‐induced phospholipase D activation in human astroglioma cells

Cited by 26 publications

References 41 publications

Multifunctional Activities of Green Tea Catechins in Neuroprotection

Multifunctional Activities of Green Tea Catechins in Neuroprotection

House Dust Mite Allergen Der f 2-induced Phospholipase D1 Activation Is Critical for the Production of Interleukin-13 through Activating Transcription Factor-2 Activation in Human Bronchial Epithelial Cells

Hippocalcin increases phospholipase D2 expression through extracellular signal‐regulated kinase activation and lysophosphatidic acid potentiates the hippocalcin‐induced phospholipase D2 expression

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Phospholipase C, protein kinase C, Ca2+/calmodulin‐dependent protein kinase II, and redox state are involved in epigallocatechin gallate‐induced phospholipase D activation in human astroglioma cells

Cited by 26 publications

References 41 publications

Multifunctional Activities of Green Tea Catechins in Neuroprotection

Multifunctional Activities of Green Tea Catechins in Neuroprotection

House Dust Mite Allergen Der f 2-induced Phospholipase D1 Activation Is Critical for the Production of Interleukin-13 through Activating Transcription Factor-2 Activation in Human Bronchial Epithelial Cells

Hippocalcin increases phospholipase D2 expression through extracellular signal‐regulated kinase activation and lysophosphatidic acid potentiates the hippocalcin‐induced phospholipase D2 expression

Contact Info

Product

Resources

About

Phospholipase C, protein kinase C, Ca²⁺/calmodulin‐dependent protein kinase II, and redox state are involved in epigallocatechin gallate‐induced phospholipase D activation in human astroglioma cells