蛋白激酶c调节脊髓神经元突起的生长

Yang, Ping; Li, Zhenqiang; Lin, Shiu‐Ru; Yin, Yuqin

doi:10.1007/s12264-010-1105-y

Cited by 12 publications

(11 citation statements)

References 36 publications

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“…Besides the β-amyloid pathology, activated PKC also inhibits tau hyperphosphorylation by phosphorylating and inactivating glycogen synthase kinase 3β (GSK3β), a central kinase phosphorylating tau (Isagawa et al, 2000). Furthermore, PKC activation has been shown to induce neurite elongation (Shirai et al, 2008;Yang et al, 2010) and synaptogenesis (Sen et al, 2016) and to restore mushroom spine synapses (Hongpaisan et al, 2013), indicating that PKC activation might even exhibit neurorestorative potential.…”

Section: Introductionmentioning

confidence: 99%

Protein kinase C -activating isophthalate derivatives mitigate Alzheimer's disease-related cellular alterations

et al. 2018

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Abnormal protein kinase C (PKC) function contributes to many pathophysiological processes relevant for Alzheimer's disease (AD), such as amyloid precursor protein (APP) processing. Phorbol esters and other PKC activators have been demonstrated to enhance the secretion of soluble APPα (sAPPα), reduce the levels of β-amyloid (Aβ), induce synaptogenesis, and promote neuroprotection. We have previously described isophthalate derivatives as a structurally simple family of PKC activators. Here, we characterised the effects of isophthalate derivatives HMI-1a3 and HMI-1b11 on neuronal viability, neuroinflammatory response, processing of APP and dendritic spine density and morphology in in vitro. HMI-1a3 increased the viability of embryonic primary cortical neurons and decreased the production of the pro-inflammatory mediator TNFα, but not that of nitric oxide, in mouse neuron-BV2 microglia co-cultures upon LPS- and IFN-γ-induced neuroinflammation. Furthermore, both HMI-1a3 and HMI-1b11 increased the levels of sAPPα relative to total sAPP and the ratio of Aβ42/Aβ40 in human SH-SY5Y neuroblastoma cells. Finally, bryostatin-1, but not HMI-1a3, increased the number of mushroom spines in proportion to total spine density in mature mouse hippocampal neuron cultures. These results suggest that the PKC activator HMI-1a3 exerts neuroprotective functions in the in vitro models relevant for AD by reducing the production of TNFα and increasing the secretion of neuroprotective sAPPα.

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Section: Introductionmentioning

confidence: 99%

Protein kinase C -activating isophthalate derivatives mitigate Alzheimer's disease-related cellular alterations

et al. 2018

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“…A third possibility is that another, pkA‐independent, signaling pathway might exist that compensates for the lack of pkA signaling in KT5720‐treated lizard RGC growth cones. Indeed, there is mounting evidence for an important role of the protein kinase C pathway in axon regeneration (Bonnici and Kapfhammer, ; Samara et al, ; Yang et al, ). Finally, it appears likely that the lizard RGC neurons would have been conditioned toward axon regeneration by the optic nerve lesion preceding our in vivo regeneration experiments.…”

Section: Discussionmentioning

confidence: 99%

Nogo‐A does not inhibit retinal axon regeneration in the lizard Gallotia galloti

Lang

Romero-Aleman

Dobson

et al. 2016

J of Comparative Neurology

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The myelin-associated protein Nogo-A contributes to the failure of axon regeneration in the mammalian central nervous system (CNS). Inhibition of axon growth by Nogo-A is mediated by the Nogo-66 receptor (NgR). Nonmammalian vertebrates, however, are capable of spontaneous CNS axon regeneration, and we have shown that retinal ganglion cell (RGC) axons regenerate in the lizard Gallotia galloti. Using immunohistochemistry, we observed spatiotemporal regulation of Nogo-A and NgR in cell bodies and axons of RGCs during ontogeny. In the adult lizard, expression of Nogo-A was associated with myelinated axon tracts and upregulated in oligodendrocytes during RGC axon regeneration. NgR became upregulated in RGCs following optic nerve injury. In in vitro studies, Nogo-A-Fc failed to inhibit growth of lizard RGC axons. The inhibitor of protein kinase A (pkA) activity KT5720 blocked growth of lizard RGC axons on substrates of Nogo-A-Fc, but not laminin. On patterned substrates of Nogo-A-Fc, KT5720 caused restriction of axon growth to areas devoid of Nogo-A-Fc. Levels of cyclic adenosine monophosphate (cAMP) were elevated over sustained periods in lizard RGCs following optic nerve lesion. We conclude that Nogo-A and NgR are expressed in a mammalian-like pattern and are upregulated following optic nerve injury, but the presence of Nogo-A does not inhibit RGC axon regeneration in the lizard visual pathway. The results of outgrowth assays suggest that outgrowth-promoting substrates and activation of the cAMP/pkA signaling pathway play a key role in spontaneous lizard retinal axon regeneration in the presence of Nogo-A. Restriction of axon growth by patterned Nogo-A-Fc substrates suggests that Nogo-A may contribute to axon guidance in the lizard visual system. J. Comp. Neurol. 525:936-954, 2017. © 2016 Wiley Periodicals, Inc.

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“…There are two compounds, BIX02188 and BIX02189, that have been reported to selectively inhibit MEK5 (Tatake et al, 2008), while more recently a selective inhibitor of ERK5, XMD8-98 has also been reported (P. . XMD8-98 does however have some off target activity, including against LRRK2 (Deng et al, 2011;P. Yang et al, 2010), a kinase important in Parkinson's disease, making the use of XMD8-98 in parallel with either BIX02188 or BIX02189 desirable for the study of ERK5 in neurons.…”

Section: Mapk Pathway Inhibitorsmentioning

confidence: 99%

“…Around the same time other microbial metabolites e the K252 compounds e were found to have similar activities Nakanishi et al, 1986), and to have some limited selectivity between PKC and PKA (Kase et al, 1987). This spawned a class of molecules known as bisindolylmaleimides (Davis et al, 1992;Toullec et al, 1991) (Table 2) that have been widely used (Yaguchi et al, 2010;P. Yang et al, 2010), as 'selective' PKC inhibitors.…”

Section: Pkc Inhibitorsmentioning

confidence: 99%

Selective kinase inhibitors as tools for neuroscience research

Martin

Arthur

2012

Neuropharmacology

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蛋白激酶c调节脊髓神经元突起的生长

Abstract: PKC activity may be important in regulating neurite outgrowth in spinal cord neurons, and betaII isoform of PKC probably plays a major role in this process.

Cited by 12 publications

References 36 publications

Protein kinase C -activating isophthalate derivatives mitigate Alzheimer's disease-related cellular alterations

Protein kinase C -activating isophthalate derivatives mitigate Alzheimer's disease-related cellular alterations

Nogo‐A does not inhibit retinal axon regeneration in the lizard Gallotia galloti

Selective kinase inhibitors as tools for neuroscience research

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