P049. Cannabinoid-mediated nitric oxide signal transduction in N18TG2 neuronal cells

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 33
Author(s):  
Derek C. Norford ◽  
Skyla T. Carney ◽  
Vicky I. Arrington ◽  
Jenelle D. Jones ◽  
Michael L. Lloyd ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Neuronal Cells

scholarly journals Melatonin and Microglia

2021 ◽  
Vol 22 (15) ◽  
pp. 8296
Author(s):  
Rüdiger Hardeland
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Signal Transduction ◽  
Endothelial Cells ◽  
Bacterial Infections ◽  
Melatonin Receptors ◽  
Sterile Inflammation ◽  
High Complexity ◽  
Anti Inflammatory ◽  
Multiple Signaling

Melatonin interacts in multiple ways with microglia, both directly and, via routes of crosstalk with astrocytes and neurons, indirectly. These effects of melatonin are of relevance in terms of antioxidative protection, not only concerning free-radical detoxification, but also in prevention of processes that cause, promote, or propagate oxidative stress and neurodegeneration, such as overexcitation, toxicological insults, viral and bacterial infections, and sterile inflammation of different grades. The immunological interplay in the CNS, with microglia playing a central role, is of high complexity and includes signaling toward endothelial cells and other leukocytes by cytokines, chemokines, nitric oxide, and eikosanoids. Melatonin interferes with these processes in multiple signaling routes and steps. In addition to canonical signal transduction by MT1 and MT2 melatonin receptors, secondary and tertiary signaling is of relevance and has to be considered, e.g., via the upregulation of sirtuins and the modulation of pro- and anti-inflammatory microRNAs. Many details concerning the modulation of macrophage functionality by melatonin are obviously also applicable to microglial cells. Of particular interest is the polarization toward M2 subtypes instead of M1, i.e., in favor of being anti-inflammatory at the expense of proinflammatory activities, which is well-documented in macrophages but also applies to microglia.

scholarly journals Inhibition of neuronal nitric-oxide synthase by phosphorylation at Threonine1296 in NG108-15 neuronal cells

FEBS Letters ◽  
2005 ◽  
Vol 579 (25) ◽  
pp. 5658-5662 ◽  
Author(s):  
Tao Song ◽  
Naoya Hatano ◽  
Kodai Kume ◽  
Katsuyoshi Sugimoto ◽  
Fuminori Yamaguchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Cells ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase

scholarly journals Dissection of a Hypoxia-induced, Nitric Oxide–mediated Signaling Cascade

2009 ◽  
Vol 20 (18) ◽  
pp. 4083-4090 ◽  
Author(s):  
Pascale F. Dijkers ◽  
Patrick H. O'Farrell
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signaling Cascade ◽  
S2 Cells ◽  
Signal Transduction System ◽  
Signaling Systems ◽  
Calcium Dependent ◽  
Drosophila S2 Cells ◽  
Oxide Synthase ◽  
Multiple Signaling

Befitting oxygen's key role in life's processes, hypoxia engages multiple signaling systems that evoke pervasive adaptations. Using surrogate genetics in a powerful biological model, we dissect a poorly understood hypoxia-sensing and signal transduction system. Hypoxia triggers NO-dependent accumulation of cyclic GMP and translocation of cytoplasmic GFP-Relish (an NFκB/Rel transcription factor) to the nucleus in Drosophila S2 cells. An enzyme capable of eliminating NO interrupted signaling specifically when it was targeted to the mitochondria, arguing for a mitochondrial NO signal. Long pretreatment with an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling. However, addition shortly before hypoxia was without effect, suggesting that signaling is supported by the prior action of NOS and is independent of NOS action during hypoxia. We implicated the glutathione adduct, GSNO, as a signaling mediator by showing that overexpression of the cytoplasmic enzyme catalyzing its destruction, GSNOR, blocks signaling, whereas knockdown of this activity caused reporter translocation in the absence of hypoxia. In downstream steps, cGMP accumulated, and calcium-dependent signaling was subsequently activated via cGMP-dependent channels. These findings reveal the use of unconventional steps in an NO pathway involved in sensing hypoxia and initiating signaling.

scholarly journals Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

1996 ◽  
Vol 271 (45) ◽  
pp. 28052-28056 ◽  
Author(s):  
Christine Roméro-Graillet ◽  
Edith Aberdam ◽  
Naïma Biagoli ◽  
William Massabni ◽  
Jean-Paul Ortonne ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Ultraviolet B ◽  
Transduction Pathway ◽  
Ultraviolet B Radiation ◽  
Cgmp Signal ◽  
Human Melanocytes

scholarly journals Nitric Oxide Attenuates Signal Transduction

2001 ◽  
Vol 88 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Hong Li ◽  
Sergey Brodsky ◽  
Mary Basco ◽  
Victor Romanov ◽  
Dino A. De Angelis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction

Inducible form of nitric oxide synthase expression in rat cortical neuronal cells in vitro

2004 ◽  
Vol 17 (1) ◽  
pp. 70-76 ◽  
Author(s):  
Claire I. Small ◽  
Geoffrey A. Lyles ◽  
Kieran C. Breen
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Cells ◽  
Oxide Synthase
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