Nitric oxide sets off an antioxidant response in adrenal cells: Involvement of sGC and Nrf2 in HO-1 induction

Astort, Francisco; Mercau, María Elisa; Giordanino, Elián F.; Degese, María Sol; Caldareri, Lilian Julia; Coso, Omar A.; Cymeryng, Cora

doi:10.1016/j.niox.2013.12.006

Cited by 11 publications

(8 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many of the processes mediated by NO at this flux are proapoptotic. However, if viewed from a temporal perspective, many of the proteins activated concurrently with p53 including but not limited to binding partners of antioxidant response elements could potentially be protective in some cells (8). Nitrosation of caspases is an acute/shortterm effect of nitrosative stress that prevents apoptosis.…”

Section: Level III Nitrosative Stress Signalingmentioning

confidence: 99%

Molecular Mechanisms of Nitric Oxide in Cancer Progression, Signal Transduction, and Metabolism

Somasundaram

Basudhar

Bharadwaj

et al. 2019

Antioxidants & Redox Signaling

153

View full text Add to dashboard Cite

show abstract

Section: Level III Nitrosative Stress Signalingmentioning

confidence: 99%

Molecular Mechanisms of Nitric Oxide in Cancer Progression, Signal Transduction, and Metabolism

Somasundaram

Basudhar

Bharadwaj

et al. 2019

Antioxidants & Redox Signaling

153

View full text Add to dashboard Cite

show abstract

“…Robust evidence has shown that NO signaling cascades exert antioxidative action with cytoprotective effects in various experimental models [24][25][26]. Further, we have previously reported that BDNF-mediated neuroprotection against 3-NP involves nitric oxide synthase (NOS) activity [6].…”

Section: No/pkg-1 Pathway Is Involved In Bdnf-mediated Sestrin2 Inducmentioning

confidence: 99%

Nuclear Factor-kappaB-Dependent Sestrin2 Induction Mediates the Antioxidant Effects of BDNF Against Mitochondrial Inhibition in Rat Cortical Neurons

Chen

Yin

et al. 2015

Mol Neurobiol

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF), in addition to its neurotrophic action, also possesses antioxidant activities. However, the underlying mechanisms remain to be fully defined. Sestrin2 is a stress-responsive gene implicated in the cellular defense against oxidative stress. Currently, the potential functions of sestrin2 in nervous system, in particular its correlation with neurotrophic factors, have not been well established. In this study, we hypothesized that BDNF may enhance sestrin2 expression to confer neuronal resistance against oxidative stress induced by 3-nitropropionic acid (3-NP), an irreversible mitochondrial complex II inhibitor, and characterized the molecular mechanisms underlying BDNF induction of sestrin2 in primary rat cortical cultures. We found that BDNF-mediated sestrin2 expression in cortical neurons required formation of nitric oxide (NO) with subsequent production of 3',5'-cyclic guanosine monophosphate (cGMP) and activation of cGMP-dependent protein kinase (PKG). BDNF induced localization of nuclear factor-kappaB (NF-κB) subunits p65 and p50 into neuronal nuclei that required PKG activities. Interestingly, BDNF exposure led to formation of a protein complex containing at least PKG-1 and p65/p50, which bound to sestrin2 promoter with resultant upregulation of its protein products. Finally, BDNF preconditioning mitigated production of reactive oxygen species (ROS) as a result of 3-NP exposure; this antioxidative effect of BDNF was dependent upon PKG activity, NF-κB, and sestrin2. Taken together, our results indicated that BDNF enhances sestrin2 expression to confer neuronal resistance against oxidative stress induced by 3-NP through attenuation of ROS formation; furthermore, BDNF induction of sestrin2 requires activation of a pathway involving NO/PKG/NF-κB.

show abstract

“…Moreover, eNOS is thought to protect against neuronal damage under hypoxic or ischemic conditions . In part, this is by helping to maintain cerebral blood flow and in part, nitric oxide, acting through cyclic GMP and the Nrf2 (nuclear factor [erythroid‐derived 2]‐like 2) transcription factor, induces antioxidant enzymes and proteins including heme oxygenase‐1 and sestrin2 . Endothelial nitric oxide facilitates mitochondrial biogenesis and the production of ATP, potentially correcting for mitochondrial dysfunction and impaired brain energetics as diatheses for migraine.…”

Section: Components Of Migraine Through the Lens Of Neuroprotectionmentioning

confidence: 99%

“…68 In part, this is by helping to maintain cerebral blood flow 69 and in part, nitric oxide, acting through cyclic GMP and the Nrf2 (nuclear factor [erythroid-derived 2]-like 2) transcription factor, induces antioxidant enzymes and proteins including heme oxygenase-1 and sestrin2. [70][71][72] Endothelial nitric oxide facilitates mitochondrial biogenesis and the production of ATP, 73 potentially correcting for mitochondrial dysfunction 22 and impaired brain energetics 23-25 as diatheses for migraine. And endothelial nitric oxide can also induce angiogenesis, 74 and the proliferation and migration of neural progenitor cells, 75 components of tissue repair.…”

Section: Components Of Migraine Through the Lens Of Neuroprotectionmentioning

confidence: 99%

The Migraine Attack as a Homeostatic, Neuroprotective Response to Brain Oxidative Stress: Preliminary Evidence for a Theory

Borkum

2017

Headache

View full text Add to dashboard Cite

Background.-Previous research has suggested that migraineurs show higher levels of oxidative stress (lipid peroxides) between migraine attacks and that migraine triggers may further increase brain oxidative stress. Oxidative stress is transduced into a neural signal by the TRPA1 ion channel on meningeal pain receptors, eliciting neurogenic inflammation, a key event in migraine. Thus, migraines may be a response to brain oxidative stress.Results.-In this article, a number of migraine components are considered: cortical spreading depression, platelet activation, plasma protein extravasation, endothelial nitric oxide synthesis, and the release of serotonin, substance P, calcitonin gene-related peptide, and brain-derived neurotrophic factor. Evidence is presented from in vitro research and animal and human studies of ischemia suggesting that each component has neuroprotective functions, decreasing oxidant production, upregulating antioxidant enzymes, stimulating neurogenesis, preventing apoptosis, facilitating mitochondrial biogenesis, and/or releasing growth factors in the brain. Feedback loops between these components are described. Limitations and challenges to the model are discussed.Conclusions.-The theory is presented that migraines are an integrated defensive, neuroprotective response to brain oxidative stress.

show abstract

Nitric oxide sets off an antioxidant response in adrenal cells: Involvement of sGC and Nrf2 in HO-1 induction

Cited by 11 publications

References 53 publications

Molecular Mechanisms of Nitric Oxide in Cancer Progression, Signal Transduction, and Metabolism

Molecular Mechanisms of Nitric Oxide in Cancer Progression, Signal Transduction, and Metabolism

Nuclear Factor-kappaB-Dependent Sestrin2 Induction Mediates the Antioxidant Effects of BDNF Against Mitochondrial Inhibition in Rat Cortical Neurons

The Migraine Attack as a Homeostatic, Neuroprotective Response to Brain Oxidative Stress: Preliminary Evidence for a Theory

Contact Info

Product

Resources

About