Involvement of protein kinase C in nerve growth factor- and K-252a-stimulated calcium uptake into PC12 cells

Dickens, Geneva; Lavarreda, Miriam; Zheng, Wenhua; Guroff, Gordon

doi:10.1002/(sici)1097-4547(19970201)47:3<271::aid-jnr5>3.0.co;2-f

Cited by 7 publications

(5 citation statements)

References 32 publications

(38 reference statements)

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“…Protein kinase C is activated by treatment of PC12 cells with NGF (Hama et al 1986;Kondratyev et al 1990), and the involvement of kinase C has been shown in several of the actions of NGF on its target cells (Balbi and Allen 1994;Perrone-Bizzozero et al 1993). Protein kinase C␣, specifically, has been implicated in the NGF-stimulated uptake of 45 Ca 2ϩ into PC12 cells (Dickens et al 1997). Figure 6A shows that chronic treatment of PC12 cells with 1 M PMA, which has been shown to down-regulate protein kinase C in PC12 cells, largely prevented the NGF-induced increase in calcium current.…”

Section: R E S U L T Smentioning

confidence: 97%

“…Experiments using radiolabeled 45 Ca 2ϩ have demonstrated (Nikodijevic and Guroff 1991) that NGF produces an increase in calcium uptake into PC12 cells. Such stimulation of calcium uptake involves a phosphorylation reaction (Nikodijevic and Guroff 1992) and protein kinase C (Dickens et al 1997). Recent studies indicate that both p140 trk and p75 NGFR will support increased calcium uptake into the cells (Jiang et al 1997).…”

Section: Introductionmentioning

confidence: 99%

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Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

Jia

Li²,

Liu

et al. 1999

Journal of Neurophysiology

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Whole cell calcium currents were recorded from PC12 cells with the perforated patch technique. Currents were evoked by step depolarization from a holding potential of -90 mV. Nerve growth factor (NGF) increased calcium currents through L-type calcium channels by >75% within 3-5 min. This increase was inhibited by K-252a, by nifedipine, and by inhibition or down-regulation of kinase C. Brain-derived neurotrophic factor (BDNF) also increased calcium current, but to a smaller extent. Thus increases in calcium current can be linked to activation of either the high- or the low-affinity nerve growth factor receptor. Increases in presynaptic calcium uptake appear to be a crucial element in the short-term actions of the neurotrophins on neurotransmitter release leading to long-term potentiation. Also, the control of calcium uptake is likely to be an important factor in the long-term actions of the neurotrophins on neuronal survival and neuronal protection. The present data indicate that the PC12 cell may be a useful model for studying the effect of the neurotrophins on calcium uptake.

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Section: R E S U L T Smentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

Jia

Li²,

Liu

et al. 1999

Journal of Neurophysiology

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“…The strength of the NGF-induced increase in calcium uptake is dependent on the intracellular calcium concentration (32); calcium uptake is greater in cells depleted of calcium and weaker in cells in which calcium levels are raised. Protein kinase C appears to participate in the process of NGF-induced calcium uptake (33). K-252a, a kinase inhibitor that blocks the actions of NGF on PC12 cells (34), mimics the action of NGF on calcium uptake (30,35) and may employ the same signaling elements as does NGF, including protein kinase C and, perhaps, the high affinity NGF receptor itself.…”

mentioning

confidence: 99%

Nerve Growth Factor (NGF)-induced Calcium Influx and Intracellular Calcium Mobilization in 3T3 Cells Expressing NGF Receptors

Jiang

Takeda

Lazarovici

et al. 1999

Journal of Biological Chemistry

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The neurotrophins have been implicated in the acute regulation of synaptic plasticity. Neurotrophin-stimulated presynaptic calcium uptake appears to play a key role in this process. To understand the mechanism of neurotrophin-stimulated calcium uptake, the regulation of calcium uptake and intracellular mobilization by nerve growth factor (NGF) was investigated using NIH 3T3 cells stably transfected with either the high affinity NGF receptor p140 trk (3T3-Trk) or the low affinity NGF receptor p75 NGFR (3T3-p75). In 3T3-Trk cells, NGF increased both calcium uptake and intracellular calcium mobilization. In 3T3-p75 cells, NGF increased calcium uptake but not intracellular calcium mobilization. K-252a alone increased intracellular calcium in 3T3-Trk cells but not in 3T3-p75 cells. Nifedipine, an inhibitor of calcium uptake through L-type calcium channels, inhibited the action of NGF on both 3T3-Trk cells and 3T3-p75 cells, indicating that both p140trk and p75 NGFR receptors are linked to nifedipine-sensitive L-type calcium channels. These studies show that either NGF receptor will support increases in intracellular calcium but that p140 trk does so by increasing both uptake and mobilization, whereas p75 NGFR does so by increasing uptake only.

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“…Recently, the availability of Gö 6976, a PKC antagonist that acts selectively on the classical (α, β, and γ) isoforms (Martiny‐Baron et al, 1993), has raised the possibility of the study of the role of these isoforms in neurotrophin‐induced signaling. Using this reagent, Dickens et al (1997) suggested that PKCα was involved in NGF‐stimulated calcium uptake in PC12 cells.…”

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confidence: 99%

Gö 6976 Is a Potent Inhibitor of Neurotrophin‐Receptor Intrinsic Tyrosine Kinase

Behrens

Strasser

Choi

1999

Journal of Neurochemistry

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Abstract:We report here that addition of the protein kinase C inhibitor Gö 6976 blocked neurotrophin-induced signaling and autophosphorylation of neurotrophin-specific tyrosine kinase (Trk) receptors, either Trk B in cortical neurons or Trk A in GT1-1-trk9 cells. The effect of Gö 6976 on Trk autophosphorylation was not inhibited by 100 M orthovanadate, suggesting that the block was not due to the activation of tyrosine phosphatases. Moreover, addition of 10 -100 nM concentrations of Gö 6976 inhibited either Trk B or Trk A intrinsic kinase activity in cell-free assays. Gö 6976 also blocked the ability of brain-derived neurotrophic factor to promote cortical neuronal survival and the ability of nerve growth factor to promote PC12 cell survival and differentiation. These results suggest that Gö 6976, besides its known inhibitory effects on lipid-and calcium-dependent isoforms of protein kinase C, can also inhibit neurotrophin signaling by directly inhibiting the intrinsic Trk. Key Words: Protein kinase C-Trk-Cortical neurons-PC12 cells-GT1-1-trk9 cells. J. Neurochem. 72, 919 -924 (1999).

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Involvement of protein kinase C in nerve growth factor- and K-252a-stimulated calcium uptake into PC12 cells

Cited by 7 publications

References 32 publications

Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

Nerve Growth Factor (NGF)-induced Calcium Influx and Intracellular Calcium Mobilization in 3T3 Cells Expressing NGF Receptors

Gö 6976 Is a Potent Inhibitor of Neurotrophin‐Receptor Intrinsic Tyrosine Kinase

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