Proteomic profile of aminoglutethimide-induced apoptosis in HL-60 cells: Role of myeloperoxidase and arylamine free radicals

Khan, Sumsullah; Baghdasarian, Argishti; Nagar, Prarthna H.; Fahlman, Richard P.; Jurasz, Paul; Michail, Karim; Aljuhani, Naif; Siraki, Arno G.

doi:10.1016/j.cbi.2015.06.020

Cited by 25 publications

(12 citation statements)

References 32 publications

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“…Each lane on the gel was excised into 12 equal pieces after being de-stained using 100 mM NH 4 HCO 3 /acetonitrile (50:50). Each gel piece was subjected to in-gel tryptic digestion as previously described 22 . The final extracted peptides from the gel were suspended in 5% acetonitrile and 1% formic acid then analyzed on an LTQ Oribitrap XL, with the resulting data being searched against the Rattus norvegicus protein database using Proteome Discoverer 1.3 as previously described 23 .…”

Section: Methodsmentioning

confidence: 99%

2-Methoxyestradiol protects against pressure overload-induced left ventricular hypertrophy

Maayah

Levasseur

Piragasam

et al. 2018

Sci Rep

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Numerous experimental studies have supported the evidence that 2-methoxyestradiol (2 ME) is a biologically active metabolite that mediates multiple effects on the cardiovascular system, largely independent of the estrogen receptor. 2 ME is a major cytochrome P450 1B1 (CYP1B1) metabolite and has been reported to have vasoprotective and anti-inflammatory actions. However, whether 2 ME would prevent cardiac hypertrophy induced by abdominal aortic constriction (AAC) has not been investigated yet. Therefore, the overall objectives of the present study were to elucidate the potential antihypertrophic effect of 2 ME and explore the mechanism(s) involved. Our results showed that 2 ME significantly inhibited AAC-induced left ventricular hypertrophy using echocardiography. The antihypertrophic effect of 2 ME was associated with a significant inhibition of CYP1B1 and mid-chain hydroxyeicosatetraenoic acids. Based on proteomics data, the protective effect of 2 ME is linked to the induction of antioxidant and anti-inflammatory proteins in addition to the modulation of proteins involved in myocardial energy metabolism. In vitro, 2 ME has shown a direct antihypertrophic effect through mitogen-activated protein kinases- and nuclear factor-κB-dependent mechanisms. The present work shows a strong evidence that 2 ME protects against left ventricular hypertrophy. Our data suggest the potential of repurposing 2 ME as a selective CYP1B1 inhibitor for the treatment of heart failure.

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Section: Methodsmentioning

confidence: 99%

2-Methoxyestradiol protects against pressure overload-induced left ventricular hypertrophy

Maayah

Levasseur

Piragasam

et al. 2018

Sci Rep

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“…Each lane was subsequently cut into 15 equal bands, with each band corresponding to a region of the gel containing proteins of a distinct molecular weight range. Each of the gel fractions was subjected to in‐gel tryptic digestion as previously described ; the resulting extracted peptides were then dried and suspended in 60 μL of 0.2% formic acid in 5% ACN.…”

Section: Methodsmentioning

confidence: 99%

Proteomic characterization of EL4 lymphoma‐derived tumors upon chemotherapy treatment reveals potential roles for lysosomes and caspase‐6 during tumor cell death in vivo

et al. 2017

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The murine mouse lymphoblastic lymphoma cell line (EL4) tumor model is an established in vivo apoptosis model for the investigation of novel cancer imaging agents and immunological treatments due to the rapid and significant response of the EL4 tumors to cyclophosphamide and etoposide combination chemotherapy. Despite the utility of this model system in cancer research, little is known regarding the molecular details of in vivo tumor cell death. Here, we report the first in-depth quantitative proteomic analysis of the changes that occur in these tumors upon cyclophosphamide and etoposide treatment in vivo. Using a label-free quantitative proteomic approach a total of 5838 proteins were identified in the treated and untreated tumors, of which 875 were determined to change in abundance with statistical significance. Initial analysis of the data reveals changes that may have been predicted, such as the downregulation of ribosomes, but demonstrates the robustness of the dataset. Analysis of the dataset also reveals the unexpected downregulation of caspase-3 and an upregulation of caspase-6 in addition to a global upregulation of lysosomal proteins in the bulk of the tumor.

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“…In-gel digestion was conducted by using trypsin (6 ng/uL) overnight (~16 h). Two steps extraction procedure was then carried out to extract the tryptic peptides from the gel (step-1: extraction by 97% water/2% acetonitrile/1% formic acid solution; step-2: extraction by 1:1 extraction buffer and acetonitrile) [1] , [3] .…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

“…A precursor mass tolerance of 10 ppm and a fragment mass tolerance of 0.8 Da were used as search parameters. Peptides were searched with carbamidomethyl cysteine as a static modification and oxidized methionine, 13 C-lysine and 13 C-arginine as dynamic modifications [1] , [3] .…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells

et al. 2016

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Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and oxygen) is known to produce H2O2. This reaction induces oxidative stress culminating in necrotic cell death in HL-60 cells (a human promyelocytic leukemia cell line). The changes in protein levels have been quantified using global proteome expression changes through stable isotope labeling by amino acids in cell culture (SILAC) followed by LC–MS/MS analysis. A total of 1459 and 1712 proteins were identified in forward and reverse experiments, respectively. However, only 390 proteins were reproducibly identified in both samples. These 390 proteins were taken into account for further analysis which has been described in “Cytoprotective effect of isoniazid against H2O2 derived injury in HL-60 cells” [1].

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Proteomic profile of aminoglutethimide-induced apoptosis in HL-60 cells: Role of myeloperoxidase and arylamine free radicals

Cited by 25 publications

References 32 publications

2-Methoxyestradiol protects against pressure overload-induced left ventricular hypertrophy

2-Methoxyestradiol protects against pressure overload-induced left ventricular hypertrophy

Proteomic characterization of EL4 lymphoma‐derived tumors upon chemotherapy treatment reveals potential roles for lysosomes and caspase‐6 during tumor cell death in vivo

Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells

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