Regulation of neurite outgrowth mediated by neuronal calcium sensor-1 and inositol 1,4,5-trisphosphate receptor in nerve growth cones

Iketani, Masumi; Imaizumi, C.; Nakamura, Fumio; Jeromin, Andreas; Mikoshiba, Katsuhiko; Goshima, Yoshio; Takei, Kohtaro

doi:10.1016/j.neuroscience.2009.04.019

Cited by 39 publications

(22 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is known that IP 3 is a ubiquitous second messenger responsible for the release of Ca 2+ from the ER, and that control of Ca 2+ by IP 3 receptors on the ER is critically important in maintaining a number of cellular functions, including cell growth, neurite outgrowth [33], [34]. Interestingly, it has been reported that calcium signaling mediated by IP 3 receptors resulted in neurite outgrowth, suggesting that IP 3 -mediated Ca 2+ release from internal stores is necessary to maintain [Ca 2+ ] i , within the optimum range of neurite outgrowth [35].…”

Section: Discussionmentioning

confidence: 99%

Neurite Outgrowth Mediated by Translation Elongation Factor eEF1A1: A Target for Antiplatelet Agent Cilostazol

Hashimoto

Ishima

2011

PLoS ONE

View full text Add to dashboard Cite

Cilostazol, a type-3 phosphodiesterase (PDE3) inhibitor, has become widely used as an antiplatelet drug worldwide. A recent second Cilostazol Stroke Prevention Study demonstrated that cilostazol is superior to aspirin for prevention of stroke after an ischemic stroke. However, its precise mechanisms of action remain to be determined. Here, we report that cilostazol, but not the PDE3 inhibitors cilostamide and milrinone, significantly potentiated nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. Furthermore, specific inhibitors for the endoplasmic reticulum protein inositol 1,4,5-triphosphate (IP3) receptors and several common signaling pathways (PLC-γ, PI3K, Akt, p38 MAPK, and c-Jun N-terminal kinase (JNK), and the Ras/Raf/ERK/MAPK) significantly blocked the potentiation of NGF-induced neurite outgrowth by cilostazol. Using a proteomics analysis, we identified that levels of eukaryotic translation elongation factor eEF1A1 protein were significantly increased by treatment with cilostazol, but not cilostamide, in PC12 cells. Moreover, the potentiating effects of cilostazol on NGF-induced neurite outgrowth were significantly antagonized by treatment with eEF1A1 RNAi, but not the negative control of eEF1A1. These findings suggest that eEF1A1 and several common cellular signaling pathways might play a role in the mechanism of cilostazol-induced neurite outgrowth. Therefore, agents that can increase the eEF1A1 protein may have therapeutic relevance in diverse conditions with altered neurite outgrowth.

show abstract

Section: Discussionmentioning

confidence: 99%

Neurite Outgrowth Mediated by Translation Elongation Factor eEF1A1: A Target for Antiplatelet Agent Cilostazol

Hashimoto

Ishima

2011

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…This report showed that release from Ca 2? stores via the IP3R is crucial for the localization of NCS-1 in the growth cone (Iketani et al 2009). This data is in agreement with our data that endogenous NCS-1 is localized in the central growth cone (lamellipodia) (Supplemental Figure 1a).…”

Section: Ncs-1's Enrichment In the Neuronal Growth Conementioning

confidence: 99%

Neuronal Calcium Sensor-1 Regulation of Calcium Channels, Secretion, and Neuronal Outgrowth

2010

View full text Add to dashboard Cite

Calcium (Ca(2+)) is an important intracellular messenger underlying cell physiology. Ca(2+) channels are the main entry route for Ca(2+) into excitable cells, and regulate processes such as neurotransmitter release and neuronal outgrowth. Neuronal Calcium Sensor-1 (NCS-1) is a member of the Calmodulin superfamily of EF-hand Ca(2+) sensing proteins residing in the subfamily of NCS proteins. NCS-1 was originally discovered in Drosophila as an overexpression mutant (Frequenin), having an increased frequency of Ca(2+)-evoked neurotransmission. NCS-1 is N-terminally myristoylated, can bind intracellular membranes, and has a Ca(2+) affinity of 0.3 μM. Over 10 years ago it was discovered that NCS-1 overexpression enhances Ca(2+)-evoked secretion in bovine adrenal chromaffin cells. The mechanism was unclear, but there was no apparent direct effect on the exocytotic machinery. It was revealed, again in chromaffin cells, that NCS-1 regulates voltage-gated Ca(2+) channels (Cavs) in G-Protein Coupled Receptor (GPCR) signaling pathways. This work in chromaffin cells highlighted NCS-1 as an important modulator of neurotransmission. NCS-1 has since been shown to regulate and/or directly interact with many proteins including Cavs (P/Q, N, and L), TRPC1/5 channels, GPCRs, IP3R, and PI4 kinase type IIIβ. NCS-1 also affects neuronal outgrowth having roles in learning and memory affecting both short- and long-term synaptic plasticity. It is not known if NCS-1 affects neurotransmission and synaptic plasticity via its effect on PIP2 levels, and/or via a direct interaction with Ca(2+) channels or their signaling complexes. This review gives a historical account of NCS-1 function, examining contributions from chromaffin cells, PC12 cells and other models, to describe how NCS-1's regulation of Ca(2+) channels allows it to exert its physiological effects.

show abstract

“…During neuronal circuitry development, the axonal growth cone must locate the appropriate path and target to establish correct wiring. Targeted inactivation of the IP 3 receptor in the nerve growth cone of chick dorsal root ganglion neurons results in growth cone retraction, which suggests that IP 3 receptormediated calcium release regulates neurite outgrowth [176,177]. This has been further confirmed by IP 3 imaging, which revealed that localized IP 3 production, as well as calcium release via the IP 3 receptor, induces growth cone turning towards the attractive source [178].…”

Section: Role Of Ip 3 Receptor In Dendritic Development Of Purkinje Cmentioning

confidence: 81%

Inositol 1,4,5-Trisphosphate Receptor-Mediated Calcium Release in Purkinje Cells: From Molecular Mechanism to Behavior

Goto

Mikoshiba

2011

Cerebellum

View full text Add to dashboard Cite

The inositol 1,4,5-trisphosphate (IP(3)) receptor is highly expressed in cerebellar Purkinje cells and mediates conspicuous calcium release from intracellular calcium stores. Receptor stimulation, such as through mGluR1, activates the G(q)-PLC pathway, which leads to IP(3)-induced calcium release and subsequent cellular responses, including cerebellar long-term depression in Purkinje cells. Recent studies have demonstrated the regulatory mechanisms of IP(3) receptor, revealing activation via IP(3) and Ca(2+), inactivation via high concentrations of Ca(2+), and modulation by various proteins that bind to the IP(3) receptor. Novel calcium imaging techniques and caged compounds provide analysis of calcium signals at the single spine level in relation to the induction of long-term depression. Genetically encoded indicators for calcium or IP(3) could provide alternate Ca(2+) or IP(3) imaging, in particular, for in vivo observations. IP(3)-induced calcium release participates in early development of dendritic branch formation, and loss-of-function mutations or hyper-activation could result various diseases. The IP(3) receptor plays a central role in calcium signaling in Purkinje cells, affecting a wide variety of cellular functions, including development, plasticity, maintenance of synaptic functions, and cerebellar motor control.

show abstract

Regulation of neurite outgrowth mediated by neuronal calcium sensor-1 and inositol 1,4,5-trisphosphate receptor in nerve growth cones

Cited by 39 publications

References 41 publications

Neurite Outgrowth Mediated by Translation Elongation Factor eEF1A1: A Target for Antiplatelet Agent Cilostazol

Neurite Outgrowth Mediated by Translation Elongation Factor eEF1A1: A Target for Antiplatelet Agent Cilostazol

Neuronal Calcium Sensor-1 Regulation of Calcium Channels, Secretion, and Neuronal Outgrowth

Inositol 1,4,5-Trisphosphate Receptor-Mediated Calcium Release in Purkinje Cells: From Molecular Mechanism to Behavior

Contact Info

Product

Resources

About