MAPK signaling in H9c2 cardiomyoblasts exposed to cholesterol secoaldehyde – Role of hydrogen peroxide

Laynes, Laura; Raghavamenon, Achuthan C.; D’Auvergne, Oswald; Achuthan, Vinitha; Uppu, Rao M.

doi:10.1016/j.bbrc.2010.11.070

Cited by 8 publications

(6 citation statements)

References 32 publications

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“…Likewise, 4-HNE, one of the predominant lipid-derived aldehydes formed in insulin-responsive cells during high-fat or high-glucose diets, promotes the formation of reactive oxygen and nitrogen species [ 166 ]. Cholesterol secosterol aldehydes, which are produced via the reaction of cholesterol with singlet oxygen or ozone [ 30 , 167 ], increase oxidative stress by inactivating catalase and thus promoting the accumulation of hydrogen peroxide and lipid hydroperoxides [ 168 ].…”

Section: Pathways To Cellular Stresses In Insulin Target Cellsmentioning

confidence: 99%

Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance

Onyango

2018

Oxidative Medicine and Cellular Longevity

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Insulin resistance (IR), a key component of the metabolic syndrome, precedes the development of diabetes, cardiovascular disease, and Alzheimer's disease. Its etiological pathways are not well defined, although many contributory mechanisms have been established. This article summarizes such mechanisms into the hypothesis that factors like nutrient overload, physical inactivity, hypoxia, psychological stress, and environmental pollutants induce a network of cellular stresses, stress responses, and stress response dysregulations that jointly inhibit insulin signaling in insulin target cells including endothelial cells, hepatocytes, myocytes, hypothalamic neurons, and adipocytes. The insulin resistance-inducing cellular stresses include oxidative, nitrosative, carbonyl/electrophilic, genotoxic, and endoplasmic reticulum stresses; the stress responses include the ubiquitin-proteasome pathway, the DNA damage response, the unfolded protein response, apoptosis, inflammasome activation, and pyroptosis, while the dysregulated responses include the heat shock response, autophagy, and nuclear factor erythroid-2-related factor 2 signaling. Insulin target cells also produce metabolites that exacerbate cellular stress generation both locally and systemically, partly through recruitment and activation of myeloid cells which sustain a state of chronic inflammation. Thus, insulin resistance may be prevented or attenuated by multiple approaches targeting the different cellular stresses and stress responses.

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Section: Pathways To Cellular Stresses In Insulin Target Cellsmentioning

confidence: 99%

Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance

Onyango

2018

Oxidative Medicine and Cellular Longevity

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“…In addition, membrane cholesterol and proteins could also be victimized by singlet molecular oxygen formed from triplet carbonyls leading to loss or gain of biological functions. In this regard, noteworthy are the findings by several groups767778 that cholesterol secoaldehyde formed by addition of ozone or singlet molecular oxygen to cholesterol may be implicated in atherosclerosis, Alzheimer disease, and apoptosis involving signaling pathways.…”

Section: Resultsmentioning

confidence: 99%

Excited singlet molecular O2 (1Δg) is generated enzymatically from excited carbonyls in the dark

Mano

Prado

Massari

et al. 2014

Sci Rep

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In mammalian tissues, ultraweak chemiluminescence arising from biomolecule oxidation has been attributed to the radiative deactivation of singlet molecular oxygen [O2 (1Δg)] and electronically excited triplet carbonyl products involving dioxetane intermediates. Herein, we describe evidence of the generation of O2 (1Δg) in aqueous solution via energy transfer from excited triplet acetone. This involves thermolysis of 3,3,4,4-tetramethyl-1,2-dioxetane, a chemical source, and horseradish peroxidase-catalyzed oxidation of 2-methylpropanal, as an enzymatic source. Both sources of excited carbonyls showed characteristic light emission at 1,270 nm, directly indicative of the monomolecular decay of O2 (1Δg). Indirect analysis of O2 (1Δg) by electron paramagnetic resonance using the chemical trap 2,2,6,6-tetramethylpiperidine showed the formation of 2,2,6,6-tetramethylpiperidine-1-oxyl. Using [18O]-labeled triplet, ground state molecular oxygen [18O2 (3Σg-)], chemical trapping of 18O2 (1Δg) with disodium salt of anthracene-9,10-diyldiethane-2,1-diyl disulfate yielding the corresponding double-[18O]-labeled 9,10-endoperoxide, was detected through mass spectrometry. This corroborates formation of O2 (1Δg). Altogether, photoemission and chemical trapping studies clearly demonstrate that chemically and enzymatically nascent excited carbonyl generates 18O2 (1Δg) by triplet-triplet energy transfer to ground state oxygen O2 (3Σg−), and supports the long formulated hypothesis of O2 (1Δg) involvement in physiological and pathophysiological events that might take place in tissues in the absence of light.

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“…25‐OH‐cholesterol is one of the commonly occurring oxysterols whose cytotoxic and pro‐oxidant effects are manifested through their ability to induce superoxide anion production (Björkhem and Diczfalusy, 2002; Lemaire‐Ewing et al, 2005). Thus, 25‐OH‐cholesterol has the ability to induce oxidative stress in CMCs (Laynes et al, 2011) and apoptosis in several cell types, including endothelial cells and smooth muscle cells, via the tumour suppressor protein p53 (Perales et al, 2010), an activator of pro‐apoptotic genes. Furthermore, 25‐OH‐cholesterol induces apoptosis in HepG2 cell line, although its effect is much less than other oxysterols, e.g.…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocyte apoptosis in ischaemia‐reperfusion due to the exogenous oxidants at the time of reperfusion

Rosca¹,

Matei²,

Dragan³

et al. 2012

Cell Biology International

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Various studies performed on different models have demonstrated that apoptosis occurs in ischaemic-reperfused myocardium in vivo; however, the individual contribution of ischaemia and reperfusion to CMC (cardiomyocyte) apoptosis remains uncertain. We have determined the main inducer of CMC apoptosis in ischaemia-reperfusion by exposing CMCs to either 30 min ischaemia followed by reperfusion or to 25-OH-cholesterol (25-hydroxycholesterol) for 1-3 days. Both ischaemia-reperfusion and exogenous oxidants increased the Bax/Bcl-2 ratio, a favourable effect for the apoptotic process. However, apoptosis was not observed in ischaemic CMCs in the absence of reperfusion. Moreover, reperfusion after 30 min ischaemia did not make an important contribution to CMC apoptosis in culture in terms of caspase 3 activation. In contrast, 25-OH-cholesterol promoted CMC apoptosis by a caspase 3-dependent mechanism that involved the transcriptional activation of the pro-apoptotic protein, Bax and post-translational degradation of the anti-apoptotic protein, Bcl-2. From these results, we conclude that CMC apoptosis is not induced by ischaemia per se, but by the oxidants from the surrounding environment at the time of reperfusion. These exogenous oxidants exacerbate the alterations induced by ischaemia and complete the apoptotic process at the time when ATP and glucose levels are restored.

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MAPK signaling in H9c2 cardiomyoblasts exposed to cholesterol secoaldehyde – Role of hydrogen peroxide

Cited by 8 publications

References 32 publications

Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance

Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance

Excited singlet molecular O2 (1Δg) is generated enzymatically from excited carbonyls in the dark

Cardiomyocyte apoptosis in ischaemia‐reperfusion due to the exogenous oxidants at the time of reperfusion

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