Protection Effect of GDNF and Neurturin on Photosensitized Crayfish Neurons and Glial Cells

Uzdensky, Anatoly B.; Komandirov, M. A.; Федоренко, Г. М.; Lobanov, A. V.

doi:10.1007/s12031-012-9858-6

Cited by 20 publications

(18 citation statements)

References 41 publications

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“…In fact, neurotrophic factors, nerve growth factor (NGF), and glia-derived growth factor but not brain-derived growth factor or ciliary neurotrophic factor protected glial cells (but not neurons) from PDT-induced necrosis and apoptosis. 80,81 NGF-mediated protection of glial cells from PDT-induced apoptosis was mediated by mitogen-activated protein kinase JNK. 80 Unlike another mitogen-activated protein, kinase p38 was involved in PDT-induced glial necrosis but not apoptosis.…”

Section: Pdt-induced Effect On Normal Nervous Tissuementioning

confidence: 99%

Photodynamic therapy: a review of applications in neurooncology and neuropathology

et al. 2015

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Section: Pdt-induced Effect On Normal Nervous Tissuementioning

confidence: 99%

Photodynamic therapy: a review of applications in neurooncology and neuropathology

et al. 2015

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“…MRN has been used in classical studies of mechanisms of neuronal activity and its inhibition [19,20], relationship bet w e e n n e u r o n a l a c t i v i t y a n d m e t a b o l i s m [ 2 3 ] , mechanosensory transduction [21], neuroglial interactions [22], responses of neurons and glial cells to various physical and chemical impacts [15,[23][24][25][26], and signal transduction processes in neurons and glia [15,[27][28][29][30][31][32][33][34].…”

Section: The Crayfish Stretch Receptormentioning

confidence: 99%

“…The methods of isolation of MRN, registration of neuronal activity, fluorescence microscopic and electron microscopic studies, and photosensitization have been described in detail earlier [22,[28][29][30][31][32][33][34]. Neurotrophic factors, inhibitors or activators of signaling proteins, were characterized in the papers [27][28][29][30][31][32][33][34][35]. In the recent research, we used also inhibitor of inducible NO synthase L-NIL (Sigma-Aldrich Co), MEK1/2 inhibitor U0126, and mammalian target of rapamycin (mTOR) inhibitor rapamycin (both from Alomone Labs, Israel).…”

Section: The Crayfish Stretch Receptormentioning

confidence: 99%

“…The percent of propidium iodide-stained nuclei of necrotic cells were counted in the predetermined standard field around MRN soma. Fragmented apoptotic nuclei were counted around the proximal 2-mm axon fragment, where apoptosis was more significant [22,[27][28][29][30][31][32][33][34]. One-way ANOVA was used for statistical evaluations of significant differences between various experimental groups.…”

Section: The Crayfish Stretch Receptormentioning

confidence: 99%

“…Other neurotrophic factors such as BDNF and CNTF as well as epidermal growth factor (EGF) were ineffective (Figs. 2a; 3a; and 4a) [29,32].…”

Section: Involvement Of Intercellular Signaling In Neuron and Glia Kimentioning

confidence: 99%

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Protection of the Crayfish Mechanoreceptor Neuron and Glial Cells from Photooxidative Injury by Modulators of Diverse Signal Transduction Pathways

et al. 2015

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Oxidative stress is the reason of diverse neuropathological processes. Photodynamic therapy (PDT), an effective inducer of oxidative stress, is used for cancer treatment, including brain tumors. We studied the role of various signaling pathways in photodynamic injury and protection of single neurons and satellite glial cells in the isolated crayfish mechanoreceptor. It was photosensitized with alumophthalocyanine Photosens in the presence of inhibitors or activators of various signaling proteins. PDT eliminated neuronal activity and killed neurons and glial cells. Inhibitory analysis showed the involvement of protein kinases Akt, glycogen synthase kinase-3β (GSK-3β), mammalian target of rapamycin (mTOR), mitogen-activated protein kinase kinases 1 and 2 (MEK1/2), calmodulin, calmodulin-dependent kinase II (CaMKII), adenylate cyclase, and nuclear factor NF-κB in PDT-induced necrosis of neurons. Nitric oxide (NO) and glial cell-derived neurotrophic factor (GDNF) reduced neuronal necrosis. In glial cells, protein kinases Akt, calmodulin, and CaMKII; protein kinases C and G, adenylate cyclase, and p38; and nuclear transcription factor NF-κB also mediated PDT-induced necrosis. In contrast, NO and neurotrophic factors nerve growth factor (NGF) and GDNF demonstrated anti-necrotic activity. Phospholipase Cγ, protein kinase C, GSK-3β, mTOR, NF-κB, mitochondrial permeability transition pores, and NO synthase mediated PDT-induced apoptosis of glial cells, whereas protein kinase A, tyrosine phosphatases, and neurotrophic factors NGF, GDNF, and neurturin were involved in protecting glial cells from photoinduced apoptosis. Signaling pathways that control cell survival and death differed in neurons and glia. Inhibitors or activators of some signaling pathways may be used as potential protectors of neurons and glia from photooxidative stress and following death.

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Proteome of brain glia: The molecular basis of diverse glial phenotypes

2013

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Several different types of nonneuronal glial cells with diverse phenotypes are present in the CNS, and all have distinct indispensible functions. Although glial cells primarily provide neurons with metabolic and structural support in the healthy brain, they may switch phenotype from a "resting" to a "reactive" state in response to pathological insults. Furthermore, this reactive gliosis is an invariant feature of the pathogeneses of CNS maladies. The glial proteome serves as a signature of glial phenotype, and not only executes physiological functions, but also acts as a molecular mediator of the reactive glial phenotype. The glial proteome is also involved in intra- and intercellular communications as exemplified by glia-glia and neuron-glia interactions. The utilization of authoritative proteomic tools and the bioinformatic analyses have helped to profile the brain glial proteome and explore the molecular mechanisms of diverse glial phenotypes. Furthermore, technologic innovations have equipped the field of "glioproteomics" with refined tools for studies of the expression, interaction, and function of glial proteins in the healthy and in the diseased CNS. Glioproteomics is expected to contribute to the elucidation of the molecular mechanisms of CNS pathophysiology and to the discovery of biomarkers and theragnostic targets in CNS disorders.

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Protection Effect of GDNF and Neurturin on Photosensitized Crayfish Neurons and Glial Cells

Cited by 20 publications

References 41 publications

Photodynamic therapy: a review of applications in neurooncology and neuropathology

Photodynamic therapy: a review of applications in neurooncology and neuropathology

Protection of the Crayfish Mechanoreceptor Neuron and Glial Cells from Photooxidative Injury by Modulators of Diverse Signal Transduction Pathways

Proteome of brain glia: The molecular basis of diverse glial phenotypes

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