Photodynamic inactivation of isolated crayfish neuron requires protein kinase C, PI 3-kinase and Ca2+

Bragin, Denis E; Kolosov, M. S.; Uzdensky, Anatoly B.

doi:10.1016/s1011-1344(03)00071-x

Cited by 8 publications

(13 citation statements)

References 38 publications

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“…A striking difference between SRN and satellite glial cells is that we have never observed apoptotic fragmentation of neuronal nuclei under photosensitization or treatment with diverse apoptosis inducers such as staurosporine and ionomycin, whereas it was often observed in glial cells (Uzdensky et al, 2002;Bragin et al, 2003). SRN and glial cells also differ in nuclear morphology: the SRN nucleus is significantly larger and the nuclear chromatin is much less condensed than in glial cells (Fig.…”

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 77%

“…In fact, the inhibition of tyrosine phosphorylation by genistein reduced neuron lifetime, whereas the inhibition of PTP by orthovanadate slowed photoinhibition of the SRN activity. This effect was opposite to that produced by inhibition of serine/threonine protein kinases such as protein kinase C and phosphatidylinositol 3-kinase, which had protected neurons against photoinactivation (Bragin et al, 2003). One could suggest that SRN functioning might be maintained by some factors supplied by the surrounding glial cells that were recognized by RTK.…”

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 91%

“…ATP depletion, cytosolic Ca 2ϩ , protein kinases C and phosphatidylinositol 3-kinase were shown to be involved in PDT-induced neuron inactivation (Uzdensky et al, 2000(Uzdensky et al, , 2002Bragin et al, 2003).…”

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 99%

“…Photoinhibition of firing is associated with [Ca 2ϩ ] i elevation (Uzdensky et al, 2000(Uzdensky et al, , 2002Bragin et al, 2003). One could suggest that AC involvement in the regulation of SRN firing may be related to modulation of [Ca 2ϩ ] i .…”

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 99%

“…Intercellular signals trigger intracellular signaling pathways that cooperate in producing the biological response. Protein kinase C (PKC) and phosphatidylinositol 3-kinase, the central components of two intracellular signaling pathways, have recently been shown to participate in the SRN response to PDT treatment (Bragin et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Uzdensky

Kolosov

Bragin

et al. 2004

Glia

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Neuroglial interactions are most profound during development or damage of nerve tissue. We studied the responses of crayfish stretch receptor neurons (SRN) and satellite glial cells to photosensitization with sulfonated aluminum phthalocyanine Photosens. Although Photosens was localized mainly in the glial envelope, neurons were very sensitive to photodynamic treatment. Photosensitization gradually inhibited and then abolished neuron activity. Neuronal and glial nuclei shrank. Some neurons and glial cells lost the integrity of the plasma membrane and died through necrosis after the treatment. The nuclei of other glial cells but not neurons become fragmented, indicating apoptosis. The number of glial nuclei around neuron soma increased, probably indicating proliferation for enhanced neuron protection. Adenylate cyclase (AC) inhibition by MDL-12330A, or tyrosine kinase (TK) inhibition by genistein, shortened neuron lifetime, whereas AC activation by forskolin or protein tyrosine phosphatases (PTP) inhibition by sodium orthovanadate prolonged neuronal activity. Therefore, cAMP and phosphotyrosines produced by AC and TK, respectively, protected SRN against photoinactivation. AC inhibition reduced photodamage of the plasma membrane and subsequent necrosis in neuronal and glial cells. AC activation prevented apoptosis in photosensitized glial cells and stimulated glial proliferation. TK inhibition protected neurons but not glia against photoinduced membrane permeabilization and subsequent necrosis whereas PTP inhibition more strongly protected glial cells. Therefore, both signaling pathways involving cAMP and phosphotyrosines might contribute to the maintenance of neuronal activity and the integrity of the neuronal and glial plasma membranes. Adenylate cyclase but not phosphotyrosine signaling pathways modulated glial apoptosis and proliferation under photooxidative stress.

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Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 77%

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 91%

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 99%

Section: Table 5 Effect Of Signaling Modulators On the Percentage Ofmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Uzdensky

Kolosov

Bragin

et al. 2004

Glia

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Involvement of Ca²⁺‐ and cyclic adenosine monophosphate‐mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial cells

Uzdensky

Lobanov

Bibov

et al. 2007

J of Neuroscience Research

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To investigate the mechanisms of oxidative injury of neurons and glia, we studied the photodynamic effect on isolated stretch receptor that consists of only two sensory neurons enwrapped by satellite glial cells. Photodynamic therapy (PDT), a potent inducer of oxidative stress, is a prospective method for destruction of brain tumors. PDT induced functional inactivation and necrosis of neurons, necrosis, apoptosis, and proliferation of glial cells. The roles of calmodulin, calmodulin-dependent kinase II, phospholipase C, protein kinases A and C, and phosphodiesterase in these processes were studied by using their inhibitors: fluphenazine, KN-93, D-609, H89, staurosporine, and papaverine, respectively. PDT-induced firing abolishment was enhanced by H89 or papaverine, whereas staurosporine acted oppositely. Fluphenazine or KN-93 reduced necrosis of neurons and glial cells. H89 enhanced necrosis of neurons, whereas staurosporine enhanced necrosis of glial cells. Inhibition of protein kinases A and C enhanced PDT-induced glial apoptosis. Photodynamic gliosis was prevented by KN-93 or staurosporine. These data indicate possible involvement of calmodulin and calmodulin-dependent kinase II in photoinduced necrosis of neurons and glia. Protein kinase C could protect glial cells from necrosis and apoptosis and participate in photoinduced gliosis and loss of neuronal activity. Protein kinase A maintained neuronal firing and protected neurons from photoinduced necrosis and glial cells from apoptosis. Phosphodiesterase reduced necrosis of photosensitized neurons and glia. Thus, Ca(2+)- and cAMP-mediated signaling pathways were involved in photooxidative injury of neurons and glia. Their pharmacological modulation may differently change the efficacy of photodynamic injury of neurons and glial cells.

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Differential photodynamic response of cultured cells to methylene blue and toluidine blue: role of dark redox processes

Blázquez‐Castro

Stockert

Sanz-Rodrı́guez

et al. 2009

Photochem Photobiol Sci

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Cultured cells treated with equal concentrations of thiazine photosensitizers methylene blue (MB) or toluidine blue (TB) showed a distinct photodynamic lethality, with TB being much more effective, when exposed to red light from a LED source. This effect is accounted for because of the differences in the chemical reduction of MB and TB in the intracellular environment. While TB accumulates as blue granular structures, MB does not give such a localization pattern. However, upon exposure of MB-treated cells to oxidant agents, the dye becomes clearly localized in the cytoplasm as blue granules. We propose that massive reduction of MB to its leuco form inside the cell inhibits most of the photodynamic damage, while no such reduction occurs with TB.

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Photodynamic inactivation of isolated crayfish neuron requires protein kinase C, PI 3-kinase and Ca2+

Cited by 8 publications

References 38 publications

Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Involvement of Ca²⁺‐ and cyclic adenosine monophosphate‐mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial cells

Differential photodynamic response of cultured cells to methylene blue and toluidine blue: role of dark redox processes

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Photodynamic inactivation of isolated crayfish neuron requires protein kinase C, PI 3-kinase and Ca2+

Cited by 8 publications

References 38 publications

Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment

Involvement of Ca2+‐ and cyclic adenosine monophosphate‐mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial cells

Differential photodynamic response of cultured cells to methylene blue and toluidine blue: role of dark redox processes

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Involvement of Ca²⁺‐ and cyclic adenosine monophosphate‐mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial cells