Retinal Cell Death Induced by TRPV1 Activation Involves NMDA Signaling and Upregulation of Nitric Oxide Synthases

@article{Leonelli2012RetinalCD,
  title={Retinal Cell Death Induced by TRPV1 Activation Involves NMDA Signaling and Upregulation of Nitric Oxide Synthases},
  author={Mauro Leonelli and Daniel Oliveira Martins and Luiz Roberto Giorgetti Britto},
  journal={Cellular and Molecular Neurobiology},
  year={2012},
  volume={33},
  pages={379-392}
}
The activation of the transient receptor potential vanilloid type 1 channel (TRPV1) has been correlated with oxidative and nitrosative stress and cell death in the nervous system. Our previous results indicate that TRPV1 activation in the adult retina can lead to constitutive and inducible nitric oxide synthase-dependent protein nitration and apoptosis. In this report, we have investigated the potential effects of TRPV1 channel activation on nitric oxide synthase (NOS) expression and function… 

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References

SHOWING 1-10 OF 95 REFERENCES

TRPV1 stimulation triggers apoptotic cell death of rat cortical neurons.

TRPV1 receptors modulate retinal development

TRPV1 receptors are involved in protein nitration and Müller cell reaction in the acutely axotomized rat retina.

Nitric Oxide Synthase Inhibition Delays Axonal Degeneration and Promotes the Survival of Axotomized Retinal Ganglion Cells

It is concluded that NO synthesized by retinal iNOS and cNOS plays a major role in RGC death and retrograde axonal degeneration following axotomy.

TRPV1: contribution to retinal ganglion cell apoptosis and increased intracellular Ca2+ with exposure to hydrostatic pressure.

RGC apoptosis induced by elevated hydrostatic pressure arises substantially through TRPV1, likely through the influx of extracellular Ca(2+).

Transient Receptor Potential Vanilloid Subtype 1 Mediates Microglial Cell Death In Vivo and In Vitro via Ca2+-Mediated Mitochondrial Damage and Cytochrome c Release1

This study is the first to demonstrate that microglia express TRPV1, and that activation of this receptor may contribute to microglial damage via Ca2+ signaling and mitochondrial disruption.

Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury.

Testing the hypothesis that endovanilloids produced following lipopolysaccharide (LPS) treatment activate TRPV1 and cause endoplasmic reticulum stress/GADD153 expression in lung cells, representing a mechanistic component of lung injury demonstrates that ER stress and cytotoxicity are not essential for pulmonary edema.

Direct imaging of NMDA-stimulated nitric oxide production in the retina

D diaminofluorescein-2 (DAF-2) is used to image real-time NO production in turtle retina in response to stimulation with N-methyl-D-aspartate (NMDA) and suggests that NO signal transduction may be more selective than suggested, and that NO may play significant intracellular roles in cells that produce it.

Importance of the non-selective cation channel TRPV1 for microglial reactive oxygen species generation

Transient Receptor Potential Vanilloid 1 Agonists Cause Endoplasmic Reticulum Stress and Cell Death in Human Lung Cells

It is concluded that activation of ER-bound TRPV1 and stimulation of GADD153 expression via the EIF2 αK3/EIF2α pathway represents a common mechanism for cytotoxicity by cell-permeable TRpV1 agonists.
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