Rémy Bosviel

University of California, Davis

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Yves‐Jean Bignon

Centre Jean Perrin

Dominique Bernard-Gallon

Centre Jean Perrin

Nadège Rabiau

Clinical Investigation Center Plurithematic Tours

Luc Fontana

Université Claude Bernard Lyon 1

Li Zhang

Loma Linda University

Samir Satih

Centre de Recherche en Nutrition Humaine d'Auvergne

Laurent Guy

Centre Hospitalier Universitaire de Clermont-Ferrand

Sean M. Wilson

Loma Linda University

John W. Newman

University of California, Davis

Cécile Gladine

Centre de Recherche en Nutrition Humaine d'Auvergne

Cooperative Institutions

Loma Linda University

Université Clermont Auvergne

Centre Jean Perrin

Centre de Recherche en Nutrition Humaine d'Auvergne

Inserm

University of California, Davis

Clermont Université

Centre National de la Recherche Scientifique

Unité de Nutrition Humaine

Western Human Nutrition Research Center

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DHA-derived oxylipins, neuroprostanes and protectins, differentially and dose-dependently modulate the inflammatory response in human macrophages: Putative mechanisms through PPAR activation

Free Radical Biology and Medicine (2016)

Rémy Bosviel Laurie Joumard‐Cubizolles Giulia Chinetti Dominique Bayle Corinne Copin

Palmitoylethanolamide

Proinflammatory cytokine

Cyclopentenone

Mediator

10.1016/j.freeradbiomed.2016.12.018

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Citations (48)

MS-based Lipidomic Profiling of Oxylipins Supports Mild Inflammation in Dysmetabolic Iron Overload Syndrome Affected Patients (P08-046-19)

Current Developments in Nutrition (2019)

C. Dalle Clément Lahaye Rémy Bosviel M. Ruivard Cécile Gladine

Insulin resistance-associated hepatic iron overload, referred as dysmetabolic iron overload syndrome (DIOS) associates a mild increase of both liver and body iron stores and various components of the metabolic syndrome (MetS). DIOS occurrence is frequent and concerns up to 20% of patients with MetS. The causes and clinical relevance of DIOS are still misunderstood. Oxylipins refer to a large family of signaling lipids notably involved in the regulation of inflammation. We hypothesized that iron overload in DIOS could be associated with an altered oxylipin profile reflecting the dysregulation of inflammatory and oxidative stress status. This case-control study involved 20 subjects with DIOS (DIOS), 20 subjects with metabolic syndrome without iron overload (MetS) and 20 healthy control subjects (Healthy). Oxylipin profiling was performed in plasma of each participant using mass spectrometry (MS)-based lipidomic profiling. Univariate analysis identified eleven oxylipins significantly higher in the DIOS group in comparison with MetS and healthy subjects. These include (i) prostaglandin D2 which is produced from arachidonic acid (AA) via the cylcooxygenase action, (ii) 8-hydroxy fatty acids including 5-HETE and 15-HETE, well known mediators of inflammation derived from AA via the lipooxygenase pathway, and (iii) two oxylipins of the cytochrome P450 pathways, namely 14,15-EET and 5,6-DiHETE. Of notes, PGD2 as well as 5- and 15-HETE are mediators of inflammation. Multivariate analysis including hierarchical cluster analysis and PCA did not discriminate subjects from the different groups. Iron overload in DIOS was associated with moderate alterations of the oxylipin profile suggesting a mild inflammation, but larger sample size would be necessary to confirm results from this pilot study. This study was funded by the University Hospital of Clermont-Ferrand and by the French Society of Internal Medicine.

Oxylipin

10.1093/cdn/nzz044.p08-046-19

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Citations (2)

BRCA1 promoter methylation in peripheral blood DNA was identified in sporadic breast cancer and controls

Cancer Epidemiology (2012)

Rémy Bosviel Stéphane Garcia Guillaume Lavediaux Emilie Michard Marine Dravers

CpG site

10.1016/j.canep.2012.02.001

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Citations (59)

Gestational High‐Altitude Hypoxia and Metabolomic Reprogramming in Pulmonary Arteries from Fetal Sheep

The FASEB Journal (2020)

Eric Leslie Breanna Jones Rafael Álvarez Chiranjib Dasgupta Oliver Fiehn

Gestational high‐altitude hypoxia increases the risk of myriad diseases in human infants including pulmonary hypertension of the newborn. Fetal sheep lungs are susceptible to long‐term intrauterine hypoxia, with the lung structure and function exhibiting characteristics associated with the development of pulmonary hypertension. Previous studies showed thickening of the pulmonary arterial medial wall, dysregulation of arterial reactivity, and reduced right ventricular output in fetal lambs following exposure to high altitude long‐term hypoxia. To further explore the mechanisms associated with hypoxia‐induced aberrations in the fetal sheep lung, we examined the premise that metabolomic and proteomic changes are associated with phenotypic transformation caused by intrauterine hypoxia. To address this hypothesis, we performed metabolomic and proteomic analysis on pulmonary arteries isolated from near term fetal lambs that were exposed to intrauterine high‐altitude hypoxia (3801 m) for the latter 110+ days of pregnancy or those gestated near sea level. The data demonstrated gestational hypoxia caused a glycolytic shift, reduced fatty acid oxidation, and elevated pentose phosphate metabolism along with increased histone expression, illustrative of increases in nucleotide synthesis. Increased nucleotide synthesis in response to gestational hypoxia is suggestive of a shift towards a proliferative and synthetic phenotype, providing insight into the mechanisms related to gestational hypoxia‐mediated pulmonary remodeling and hypertension. These studies begin to shed light on the mechanistic underpinnings associated with the phenotypic transformations to the pulmonary vasculature that occur with intrauterine hypoxia. Support or Funding Information Supported in part by NIH grants HD083132 (LZ), 1U24DK097154 (OF ) through a pilot project grant to SMW and HD098477 (SMW). Additional support was provided by USDA Intramural projects #2032‐51530‐022‐00D and #2032‐51530‐025‐00D (J.W.N.). The USDA is an equal opportunity provider, and employer.

Hypoxia

Intrauterine growth restriction

Hypoxic pulmonary vasoconstriction

10.1096/fasebj.2020.34.s1.03778

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Gene Expression Profiling of Breast Cancer Cell Lines in Response to Soy Isoflavones Using a Pangenomic Microarray Approach

OMICS A Journal of Integrative Biology (2010)

Samir Satih Nasséra Chalabi Nadège Rabiau Rémy Bosviel Luc Fontana

Although the rate of breast cancer differs between women in Asian and Western countries, molecular genetics/genomics basis of this epidemiological observation remains elusive. Moreover, the intake of phytoestrogens is associated with a lower incidence of breast cancer. Genistein and daidzein are the primary soy isoflavones with a chemical structure similar to estrogens. Conceivably, the actions of phytoestrogens on gene expression signatures might mediate their postulated effects on breast cancer pathogenesis. The present study evaluated the transcriptional responsiveness of breast cancer cells to soy phytoestrogens using a whole-genome microarray-based approach. Human breast cancer cell lines and a fibrocystic breast cell line were treated with genistein or daidzein. We identified 278 and 334 differentially expressed genes after genistein or daidzein treatment, respectively, in estrogen-positive (MCF-7) and estrogen-negative (MDA-MB-231, MCF-10a) cells. Hierarchical clustering of this finding revealed a significant modulation, respectively, of 246 or 169 genes after genistein or daidzein exposures. Importantly, the molecular pathways for the differentially expressed genes included those that relate to cell communication, biodegradation of xenobiotics, lipid metabolism, signal transduction, and cell growth/death. These molecular observations collectively contribute to a growing knowledgebase on the putative mechanism(s) of action of phytoestrogens in breast cancer pathogenesis and chemoprevention.

10.1089/omi.2009.0124

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Citations (42)

Fat burning capacity in a mixed macronutrient meal protocol does not reflect metabolic flexibility in women who are overweight or obese.

medRxiv (Cold Spring Harbor Laboratory) (2024)

Mary M. Ahern Virginia M. Artegoitia Rémy Bosviel John W. Newman Nancy L. Keim

Metabolic flexibility, the ability to switch from glucose to fat as a fuel source, is considered a marker of metabolic health. Higher fat oxidation is often associated with greater flexibility and insulin sensitivity, while lower fat oxidation is linked to metabolic inflexibility and insulin resistance. However, our study challenges the universal validity of this relationship, uncovering a more nuanced understanding of the complex interplay between fuel source switching and fat oxidation, especially in the presence of insulin resistance.

10.1101/2024.08.29.24312791

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High Altitude Hypoxia Impacts Omega‐3 Fatty Acid Metabolites in Plasma of Fetal and Newborn Sheep

The FASEB Journal (2018)

Vanessa Lopez Michael La Frano Rémy Bosviel John W. Newman Richard B. Thorpe

Perinatal hypoxia has profound effect on an infant's development, with physiological impairment of multiple organ systems. The present study explored the effect of hypoxia due to long term high altitude exposure during gestation and after birth on lipid mediators by measuring the metabolites that foreshadow oxidative stress and inflammation, which are primary drivers of dysfunction. We tested the hypothesis that long term hypoxia reduces the amount of oxylipin and endocannabinoid production, which are important mediators of oxidative stress and inflammation. To test this hypothesis pregnant sheep and newborn lambs were housed at a low altitude (700 m) or exposed to an altitude of 3,800 meters starting gestation day 30. UPLC‐MS/MS analysis was used to investigate the lipid mediator composition in plasma collected from veins of near‐term fetal and newborn animals. The results show that hypoxia causes an overwhelming effect on omega‐3 fatty acids and their derivatives, which are crucial in late‐stage fetal development. Several of the omega‐3 fatty acids reduced with hypoxia have well known effects on inflammation, vascular tone, and oxidative stress. Furthermore, we tracked the origin of the identified oxylipins and endocannabinoids by tracing their pathways. The cytochrome P450 (CYP) pathway enzymes and the subsequent activity of soluble epoxide hydrolase (sEH) are prominent synthesizers of the oxylipins such as epoxyeicosatrienoic acids (EETs) and epoxyoctadecenoic acids (EpOMEs). Previous studies have suggested the role of EETs and EpOMEs in vasodilation, a feature in inflammation. Based on these findings we demonstrated that a majority of the affected oxylipins were produced from CYP and sEH enzymes, which are important to vascular function. These findings provide novel insight into our understanding of lipid metabolites to hypoxia‐induced dysfunction in the developing fetus and newborn. In the long term this may help us develop novel therapies that target inflammatory pathways induced by pre and post‐natal hypoxia. Support or Funding Information This material is based upon work supported by NIH grants P01HD083132 and 1U24DK097154 through a pilot project grant to Sean Wilson. VL is a recipient of the American Physiological Society's Short‐Term Research Education Program to Increase Diversity in Health‐Related Research (STRIDE) Fellowship funded by the APS and a grant from the National Heart, Lung and Blood Institute R25HL115473. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Oxylipin

Hypoxia

Epoxide hydrolase 2

10.1096/fasebj.2018.32.1_supplement.858.5

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Citations (1)

39: Les phyto-oestrogènes du soja déméthylent les oncosuppresseurs BRCA1 et BRCA2 dans les cellules de cancer du sein

Bulletin du Cancer (2010)

Bernard-Gallon Dominique Rémy Bosviel Nadège Rabiau Elise Dumollard Pierre Déchelotte

10.1016/s0007-4551(15)31132-2

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Genetic polymorphisms in CYP1A1, CYP1B1, COMT, GSTP1 and NAT2 genes and association with bladder cancer risk in a French cohort.

PubMed (2009)

Luc Fontana Laëtitia Delort Laurie Joumard Nadège Rabiau Rémy Bosviel

Tobacco smoking and environmental exposures are the main known risk factors for bladder cancer (BC) via exposure to chemical carcinogens. Genetic differences in the metabolism of chemicals have been suggested to be associated with individual susceptibility to BC. Polymorphisms in genes coding to metabolising enzymes, resulting in variation of carcinogen detoxification efficiency, may therefore change the response of individuals to chemical carcinogens and be associated with an increased BC risk.The aim of the study was to investigate the association between functional polymorphisms in CYP1A1, CYP1B1, COMT, GSTP1 and NAT2 genes and BC risk, through a hospital-based case-control study. The genotyping of 11 Single Nucleotide Polymorphisms (SNPs) was carried out on DNA of 51 bladder cancer male patients and 45 male controls. The technique of MGB (Minor Groove Binder) probes that utilize allelic discrimination with the Taqman(R) method was used.Individuals with NAT2 slow acetylator genotypes had a significant increase in risk of BC compared to individuals with NAT2 rapid acetylators (OR adjusted for smoking status=2.70; 95% CI, 1.10-6.61). GSTP1 Ile(105)Val variants (deletion of one - Ile/Val- and two -Val/Val-, null genotype- copies) showed a marginal increased risk of BC with OR adjusted for smoking status of 2.27 (95% CI, 0.97-5.31) compared to individuals carrying wild-type genotype (Ile/Ile). No statistically significant effects on BC risk with CYP1A1, CYP11B1 and COMT genotypes were observed.The results are consistent with previous literature among Caucasian populations.

GSTP1

Source

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Citations (59)

Epigenetic modulation ofBRCA1andBRCA2gene expression by equol in breast cancer cell lines

British Journal Of Nutrition (2012)

Rémy Bosviel Julie Durif Pierre Déchelotte Yves‐Jean Bignon Dominique Bernard-Gallon

S -Equol is a metabolite resulting from the conversion of daidzein, a soya phyto-oestrogen, by the gut microflora. The potential protective effects of equol in breast cancer are still under debate. Consequently, we investigated the effects of equol on DNA methylation of breast cancer susceptibility genes ( BRCA1 and BRCA2 ) and oncosuppressors in breast cancer cell lines (MDA-MB-231 and MCF-7) and in a dystrophic breast cell line (MCF-10a) following exposure to S -equol (2 μ m ) for 3 weeks. We demonstrated by quantitative analysis of methylated alleles a significant decrease in the methylation of the cytosine phosphate guanine (CpG) islands in the promoters of BRCA1 and BRCA2 after the S -equol treatment in MCF-7 and MDA-MB-231 cells and a trend in MCF-10a cells. We also showed that S -equol increases BRCA1 and BRCA2 protein expression in the nuclei and the cytoplasm in MCF-7, MDA-MB-231 and MCF-10a cell lines by immunohistochemistry. The increase in BRCA1 and BRCA2 proteins was also found after Western blotting in the studied cell lines. In summary, we demonstrated the demethylating effect of S -equol on the CpG islands inside the promoters of BRCA1 and BRCA2 genes, resulting in an increase in the level of expressed oncosuppressors in breast cancer cell lines.

Equol

CpG site

Bisulfite sequencing

Demethylating agent

10.1017/s000711451100657x

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Citations (37)