Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Almeida, Ana S.; Queiroga, Cláudia S. F.; Sousa, Marcos F. Q.; Alves, Paula M.; Vieira, Helena L.A.

doi:10.1074/jbc.m111.306738

Cited by 91 publications

(98 citation statements)

References 39 publications

(67 reference statements)

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“…Exogenous application of low doses of CO can recapitulate the cytoprotective effects of HO-1 induction (20)(21)(22)(23)(24)(25)(26)(27)(28), but few studies have demonstrated that CO can actually substitute for the absence of HO-1 in a cell type-specific fashion, particularly in the brain. Only a few reports have examined the protective effects of CO on neuronal cells in vitro and in vivo (29)(30)(31)(32). In fact, the majority of reports contend that CO is potently neurotoxic, resulting in memory loss, confusion, and even flu-like symptoms thought to arise in part from neuronal cell death.…”

Section: Introductionmentioning

confidence: 99%

Microglia regulate blood clearance in subarachnoid hemorrhage by heme oxygenase-1

Schallner¹,

Pandit²,

LeBlanc³

et al. 2015

J. Clin. Invest.

159

141

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Section: Introductionmentioning

confidence: 99%

Microglia regulate blood clearance in subarachnoid hemorrhage by heme oxygenase-1

Schallner¹,

Pandit²,

LeBlanc³

et al. 2015

J. Clin. Invest.

159

141

View full text Add to dashboard Cite

“…The mechanisms by which CO mediates its effect are complex. It may have both deleterious and beneficial effects on mitochondrial biogenesis and function (6,53) as well as calcium availability (53), thereby influencing apoptosis. In addition, through its activation of p38 mitogen-activated protein (MAP) kinase, CO alters various signaling kinases and prevents apoptosis in some models (54) but may enhance it in others, as suggested by an increased eryptosis or red cell death, in the presence of a CO-releasing molecule, CORM-2 (51).…”

Section: Carbon Monoxidementioning

confidence: 99%

Signaling Function of Heme Oxygenase Proteins

Dennery

2014

Antioxidants & Redox Signaling

100

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Significance: Many reports have underscored the importance of the heme degradation pathway that is regulated by heme oxygenase (HO). This reaction releases bile pigments and carbon monoxide (CO), which are important antioxidant and signaling molecules. Thus, the reaction of HO-1 would have significant cytoprotective effects. Nevertheless, the importance of this protein goes beyond its enzymatic action. New evidence outlines significant effects of inactive forms of the HO-1 protein. Recent Advances: In fact, the role of the HO protein in cellular signaling, including transcription factor activation, binding to proteins, phosphorylation, and modulation of protein function, among others, has started being elucidated. The mechanism by which the inducible form of HO-1, in particular, can migrate to various cellular compartments to mediate important signaling or how and why it binds to key transcription factors and other proteins that are important in DNA repair is also described in several physiologic systems. Critical Issues: The signaling functions of HO-1 may have particular relevance in clinical circumstances, including cancer, as redistribution of HO-1 into the nuclear compartment is observed with cancer progression and metastasis. In addition, along with oxidative stress, the pleiotropic functions of HO-1 modulate antioxidant defense. In organ transplantation, HO and its byproducts suppress rejection at multiple levels and in sepsis-induced pulmonary dysfunction, inhaled CO or modulation of HO activity can change the course of the disease in animals. Future Directions: It is hoped that a more detailed understanding of the various signaling functions of HO will guide therapeutic approaches for complex diseases.

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“…Low Cl − KH solution (50 ml) was bubbled with CO in a glass bottle for 30 min [13]. Different dilutions were achieved by mixing the bubbled low Cl − KH solution with non-bubbled low Cl − KH solution.…”

Section: Simultaneous Measurements Of Camp and I Scmentioning

confidence: 99%

Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia

Zhang

Yip

2018

Cell Physiol Biochem

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Background/Aims: Carbon monoxide (CO) is an important gas produced endogenously by heme oxygenase (HO) that functions as an anti-inflammatory and in ion channel modulation, but the effects of CO on airway inflammation and ion transport remains unclear. Methods: The effect of CO on cell damage- and nucleotide-induced pro-inflammatory cytokine release in primary human bronchial epithelia cells (HBE) and in the 16HBE14o- human bronchial epithelial cell line were investigated. The effects of CO on calcium- and cAMP-dependent chloride (Cl^-) secretion were examined using a technique that allowed the simultaneous measurement and quantification of real-time changes in signalling molecules (cAMP and Ca²⁺) and ion transport in a polarised epithelium. Results: CO suppressed the release of interleukin (IL)-6 and IL-8 and decreased the phosphorylation of ERK1/2 and NF-κB p65. Furthermore, CO inhibited UTP-induced increases in calcium and Cl^- secretion, and forskolin-induced increases in cAMP and Cl^- secretion. Conclusions: These findings suggest a novel anti-inflammatory role of CO in human bronchial epithelia via interactions with purinergic signalling pathways. Further, CO modulated both the Ca²⁺- and cAMP-dependent secretion of Cl^-.

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Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Cited by 91 publications

References 39 publications

Microglia regulate blood clearance in subarachnoid hemorrhage by heme oxygenase-1

Microglia regulate blood clearance in subarachnoid hemorrhage by heme oxygenase-1

Signaling Function of Heme Oxygenase Proteins

Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia

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