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Article ; Online: mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema.

2024 Volume 25, Issue 3, Page(s) 1650–1684

Abstract: Lung diseases develop when telomeres shorten beyond a critical point. We constructed a mouse model in which the catalytic subunit of telomerase (mTert), or its catalytically inactive form ( ... ...

Abstract	Lung diseases develop when telomeres shorten beyond a critical point. We constructed a mouse model in which the catalytic subunit of telomerase (mTert), or its catalytically inactive form (mTert
MeSH term(s)	Mice ; Animals ; Pulmonary Emphysema ; Microvascular Rarefaction ; Telomere Shortening ; Emphysema ; Telomerase/genetics
Chemical Substances	Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2024-02-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/s44319-023-00041-1
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Increased Sirt1 secreted from visceral white adipose tissue is associated with improved glucose tolerance in obese Nrf2-deficient mice.

Braud, Laura / Pini, Maria / Stec, Donald F / Manin, Sylvie / Derumeaux, Geneviève / Stec, David E / Foresti, Roberta / Motterlini, Roberto

Redox biology

2020 Volume 38, Page(s) 101805

Abstract: Obesity is associated with metabolic dysregulation characterized by insulin resistance and glucose intolerance. Nuclear factor E2-related factor (Nrf2) is a critical regulator of the stress response and Nrf2-deficient mice ( ... ...

Abstract	Obesity is associated with metabolic dysregulation characterized by insulin resistance and glucose intolerance. Nuclear factor E2-related factor (Nrf2) is a critical regulator of the stress response and Nrf2-deficient mice (Nrf2
MeSH term(s)	Adipose Tissue, White ; Animals ; Diet, High-Fat/adverse effects ; Glucose ; Insulin Resistance/genetics ; Intra-Abdominal Fat ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; NF-E2-Related Factor 2/genetics ; Obesity/genetics ; Sirtuin 1/genetics
Chemical Substances	NF-E2-Related Factor 2 ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-11-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101805
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Article ; Online: Human and murine macrophages exhibit differential metabolic responses to lipopolysaccharide - A divergent role for glycolysis.

Vijayan, Vijith / Pradhan, Pooja / Braud, Laura / Fuchs, Heiko R / Gueler, Faikah / Motterlini, Roberto / Foresti, Roberta / Immenschuh, Stephan

Redox biology

2019 Volume 22, Page(s) 101147

Abstract: Macrophages adopt different phenotypes in response to microenvironmental changes, which can be principally classified into inflammatory and anti-inflammatory states. Inflammatory activation of macrophages has been linked with metabolic reprogramming from ...

Abstract	Macrophages adopt different phenotypes in response to microenvironmental changes, which can be principally classified into inflammatory and anti-inflammatory states. Inflammatory activation of macrophages has been linked with metabolic reprogramming from oxidative phosphorylation to aerobic glycolysis. In contrast to mouse macrophages, little information is available on the link between metabolism and inflammation in human macrophages. In the current report it is demonstrated that lipopolysaccharide (LPS)-activated human peripheral blood monocyte-derived macrophages (hMDMs) fail to undergo metabolic reprogramming towards glycolysis, but rely on oxidative phosphorylation for the generation of ATP. By contrast, activation by LPS led to an increased extracellular acidification rate (glycolysis) and decreased oxygen consumption rate (oxidative phosphorylation) in mouse bone marrow-derived macrophages (mBMDMs). Mitochondrial bioenergetics after LPS stimulation in human macrophages was unchanged, but was markedly impaired in mouse macrophages. Furthermore, treatment with 2-deoxyglucose, an inhibitor of glycolysis, led to cell death in mouse, but not in human macrophages. Finally, glycolysis appeared to be critical for LPS-mediated induction of the anti-inflammatory cytokine interleukin-10 in both human and mouse macrophages. In summary, these findings indicate that LPS-induced immunometabolism in human macrophages is different to that observed in mouse macrophages.
MeSH term(s)	Animals ; Cells, Cultured ; Cytokines/metabolism ; Energy Metabolism ; Glycolysis ; Humans ; Lipopolysaccharides/immunology ; Macrophage Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Membrane Potential, Mitochondrial ; Mice ; Oxidative Phosphorylation
Chemical Substances	Cytokines ; Lipopolysaccharides
Language	English
Publishing date	2019-02-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2213-2317
ISSN (online)	2213-2317
DOI	10.1016/j.redox.2019.101147
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Article: Platelet-Rich Plasma Improves the Wound Healing Potential of Mesenchymal Stem Cells through Paracrine and Metabolism Alterations.

Hersant, Barbara / Sid-Ahmed, Mounia / Braud, Laura / Jourdan, Maud / Baba-Amer, Yasmine / Meningaud, Jean-Paul / Rodriguez, Anne-Marie

Stem cells international

2019 Volume 2019, Page(s) 1234263

Abstract: Chronic and acute nonhealing wounds represent a major public health problem, and replacement of cutaneous lesions by the newly regenerated skin is challenging. Mesenchymal stem cells (MSC) and platelet-rich plasma (PRP) were separately tested in the ... ...

Abstract	Chronic and acute nonhealing wounds represent a major public health problem, and replacement of cutaneous lesions by the newly regenerated skin is challenging. Mesenchymal stem cells (MSC) and platelet-rich plasma (PRP) were separately tested in the attempt to regenerate the lost skin. However, these treatments often remained inefficient to achieve complete wound healing. Additional studies suggested that PRP could be used in combination with MSC to improve the cell therapy efficacy for tissue repair. However, systematic studies related to the effects of PRP on MSC properties and their ability to rebuild skin barrier are lacking. We evaluated in a mouse exhibiting 4 full-thickness wounds, the skin repair ability of a treatment combining human adipose-derived MSC and human PRP by comparison to treatment with saline solution, PRP alone, or MSC alone. Wound healing in these animals was measured at day 3, day 7, and day 10. In addition, we examined in vitro and in vivo whether PRP alters in MSC their proangiogenic properties, their survival, and their proliferation. We showed that PRP improved the efficacy of engrafted MSC to replace lost skin in mice by accelerating the wound healing processes and ameliorating the elasticity of the newly regenerated skin. In addition, we found that PRP treatment stimulated
Language	English
Publishing date	2019-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573856-2
ISSN	1687-9678 ; 1687-966X
ISSN (online)	1687-9678
ISSN	1687-966X
DOI	10.1155/2019/1234263
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Article ; Online: Adipose tissue senescence is mediated by increased ATP content after a short-term high-fat diet exposure.

Pini, Maria / Czibik, Gabor / Sawaki, Daigo / Mezdari, Zaineb / Braud, Laura / Delmont, Thaïs / Mercedes, Raquel / Martel, Cécile / Buron, Nelly / Marcelin, Geneviève / Borgne-Sanchez, Annie / Foresti, Roberta / Motterlini, Roberto / Henegar, Corneliu / Derumeaux, Geneviève

Aging cell

2021 Volume 20, Issue 8, Page(s) e13421

Abstract: In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of ... ...

Abstract	In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of WAT senescence early after initiation of high-fat diet (HFD, 1-10 weeks) in 5-month-old male C57BL/6J mice and the potential role of energy metabolism. We first showed that WAT senescence occurred 2 weeks after HFD as evidenced in whole WAT by increased senescence-associated ß-galactosidase activity and cyclin-dependent kinase inhibitor 1A and 2A expression. WAT senescence affected various WAT cell populations, including preadipocytes, adipose tissue progenitors, and immune cells, together with adipocytes. WAT senescence was associated with higher glycolytic and mitochondrial activity leading to enhanced ATP content in HFD-derived preadipocytes, as compared with chow diet-derived preadipocytes. One-month daily exercise, introduced 5 weeks after HFD, was an effective senostatic strategy, since it reversed WAT cellular senescence, while reducing glycolysis and production of ATP. Interestingly, the beneficial effect of exercise was independent of body weight and fat mass loss. We demonstrated that WAT cellular senescence is one of the earliest events occurring after HFD initiation and is intimately linked to the metabolic state of the cells. Our data uncover a critical role for HFD-induced elevated ATP as a local danger signal inducing WAT senescence. Exercise exerts beneficial effects on adipose tissue bioenergetics in obesity, reversing cellular senescence, and metabolic abnormalities.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Adipose Tissue/physiopathology ; Animals ; Diet, High-Fat/adverse effects ; Energy Metabolism/physiology ; Male ; Mice
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2021-07-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13421
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Zs.A 6581: Show issues

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Article ; Online: Platelets facilitate the wound-healing capability of mesenchymal stem cells by mitochondrial transfer and metabolic reprogramming.

Levoux, Jennyfer / Prola, Alexandre / Lafuste, Peggy / Gervais, Marianne / Chevallier, Nathalie / Koumaiha, Zeynab / Kefi, Kaouthar / Braud, Laura / Schmitt, Alain / Yacia, Azzedine / Schirmann, Aurélie / Hersant, Barbara / Sid-Ahmed, Mounia / Ben Larbi, Sabrina / Komrskova, Katerina / Rohlena, Jakub / Relaix, Frederic / Neuzil, Jiri / Rodriguez, Anne-Marie

Cell metabolism

2021 Volume 33, Issue 3, Page(s) 688–690

Language	English
Publishing date	2021-03-03
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.02.003
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Zs.A 6169: Show issues

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Article ; Online: Platelets Facilitate the Wound-Healing Capability of Mesenchymal Stem Cells by Mitochondrial Transfer and Metabolic Reprogramming.

Cell metabolism

2021 Volume 33, Issue 2, Page(s) 283–299.e9

Abstract: Platelets are known to enhance the wound-healing activity of mesenchymal stem cells (MSCs). However, the mechanism by which platelets improve the therapeutic potential of MSCs has not been elucidated. Here, we provide evidence that, upon their activation, ...

Abstract	Platelets are known to enhance the wound-healing activity of mesenchymal stem cells (MSCs). However, the mechanism by which platelets improve the therapeutic potential of MSCs has not been elucidated. Here, we provide evidence that, upon their activation, platelets transfer respiratory-competent mitochondria to MSCs primarily via dynamin-dependent clathrin-mediated endocytosis. We found that this process enhances the therapeutic efficacy of MSCs following their engraftment in several mouse models of tissue injury, including full-thickness cutaneous wound and dystrophic skeletal muscle. By combining in vitro and in vivo experiments, we demonstrate that platelet-derived mitochondria promote the pro-angiogenic activity of MSCs via their metabolic remodeling. Notably, we show that activation of the de novo fatty acid synthesis pathway is required for increased secretion of pro-angiogenic factors by platelet-preconditioned MSCs. These results reveal a new mechanism by which platelets potentiate MSC properties and underline the importance of testing platelet mitochondria quality prior to their clinical use.
MeSH term(s)	Animals ; Blood Platelets/metabolism ; Male ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria/metabolism ; Wound Healing
Language	English
Publishing date	2021-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2020.12.006
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Article ; Online: Effect of Brewing Duration on the Antioxidant and Hepatoprotective Abilities of Tea Phenolic and Alkaloid Compounds in a t-BHP Oxidative Stress-Induced Rat Hepatocyte Model.

Braud, Laura / Peyre, Ludovic / de Sousa, Georges / Armand, Martine / Rahmani, Roger / Maixent, Jean-Michel

Molecules (Basel, Switzerland)

2015 Volume 20, Issue 8, Page(s) 14985–15002

Abstract: Tea is an interesting source of antioxidants capable of counteracting the oxidative stress implicated in liver diseases. We investigated the impact of antioxidant molecules provided by a mixture of teas' leaves (green, oolong, pu-erh) after different ... ...

Abstract	Tea is an interesting source of antioxidants capable of counteracting the oxidative stress implicated in liver diseases. We investigated the impact of antioxidant molecules provided by a mixture of teas' leaves (green, oolong, pu-erh) after different infusion durations in the prevention of oxidative stress in isolated rat hepatocytes, by comparison with pure epigallocatechin-3-gallate (EGCG), the main representative of tea catechins. Dried aqueous tea extracts (ATE) obtained after 5, 15 and 30 min infusion time were characterized for total polyphenols (gallic acid equivalent), catechins, gallic acid and caffeine (HPLC-DAD/ESI-MS) contents, and for scavenging ability against 2,2-diphenyl-1-picrylhydrazyl free radical. Hepatoprotection was evaluated through hepatocyte viability tests using tert-butyl hydroperoxide as a stress inducer, (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, neutral red uptake, real-time cellular impedance) and mitochondrial function tests. We showed that a 5-min incubation time is sufficient for an optimal bioaccessibility of tea compounds with the highest antioxidative ability, which decreases for longer durations. A 4-h pretreatment of cells with ATE significantly prevented cell death by regulating reactive oxygen species production and maintaining mitochondrial integrity. Pure EGCG, at doses similar in ATE (5-12 µM), was inefficient, suggesting a plausible synergy of several water-soluble tea compounds to explain the ATE beneficial effects.
MeSH term(s)	Alkaloids/pharmacology ; Animals ; Antioxidants/pharmacology ; Caffeine/pharmacology ; Catechin/analogs & derivatives ; Catechin/pharmacology ; Cell Survival/drug effects ; Chromatography, High Pressure Liquid ; Hepatocytes/drug effects ; Hepatocytes/pathology ; Liver/drug effects ; Male ; Mitochondria/drug effects ; Mitochondria/metabolism ; Models, Biological ; Oxidative Stress/drug effects ; Phenols/pharmacology ; Plant Extracts/pharmacology ; Protective Agents/pharmacology ; Rats ; Spectrometry, Mass, Electrospray Ionization ; Superoxides/metabolism ; Tea/chemistry ; Time Factors ; tert-Butylhydroperoxide/toxicity
Chemical Substances	Alkaloids ; Antioxidants ; Phenols ; Plant Extracts ; Protective Agents ; Tea ; Superoxides (11062-77-4) ; Caffeine (3G6A5W338E) ; Catechin (8R1V1STN48) ; tert-Butylhydroperoxide (955VYL842B) ; epigallocatechin gallate (BQM438CTEL)
Language	English
Publishing date	2015-08-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules200814985
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Article: Antioxidant properties of tea blunt ROS-dependent lipogenesis: beneficial effect on hepatic steatosis in a high fat-high sucrose diet NAFLD obese rat model

Braud, Laura / Alessandro Nascimento / Catherine Riva / Cyril Reboul / Georges de Sousa / Grégory Meyer / Jean-Michel Maixent / Martine Armand / Roger Rahmani / Sandrine Gaillard / Sylvain Battault

Journal of nutritional biochemistry. 2017 Feb., v. 40

2017

Abstract: Oxidative stress could trigger lipid accumulation in liver and thus hepatic steatosis. Tea is able to prevent liver disorders, but a direct link between antioxidant capacities and prevention of steatosis has not been reported yet. We aimed to investigate ...

Abstract	Oxidative stress could trigger lipid accumulation in liver and thus hepatic steatosis. Tea is able to prevent liver disorders, but a direct link between antioxidant capacities and prevention of steatosis has not been reported yet. We aimed to investigate such relationship in a rat model of high fat-high sucrose diet (HFS)-induced obesity and to explore more deeply the mechanisms in isolated hepatocytes. Wistar rats were divided into a control group (standard diet), an HFS group (high fat-sucrose diet) and an HFS+tea group (HFS diet with ad-libitum access to tea drink). Body weight, fat mass, glycemic parameters in blood, lipid and oxidative stress parameters in blood and liver were measured in each group after 14 weeks. Isolated hepatocytes were treated with the reactive oxygen species (ROS) inducer t-BHP in the presence or not of antioxidants (tempol or tea), and superoxide anion production and lipid accumulation were measured using specific fluorescent probes. We reported that the HFS diet highly increased hepatic lipids content, while tea consumption attenuated steatosis and improved the oxidative status (decrease in hepatic oxidative stress, increase in plasma total antioxidant capacity). The role of antioxidant properties of tea in such phenomenon was confirmed in primary cultured rat hepatocytes. Indeed, the increase of mitochondrial ROS production with t-BHP resulted in lipid accumulation in hepatocytes (positive linear regression), and antioxidants (tempol or tea) normalized both. We reported that the antioxidant properties of tea protect rats from an obesogenic HFS diet-induced hepatic steatosis by counteracting the ROS-dependent lipogenesis.
Keywords	animal models ; antioxidant activity ; antioxidants ; blood composition ; diet ; fatty liver ; fluorescent dyes ; hepatocytes ; lipids ; lipogenesis ; liver ; mitochondria ; obesity ; oxidative stress ; rats ; regression analysis ; sucrose ; superoxide anion ; tea ; tea (beverage)
Language	English
Dates of publication	2017-02
Size	p. 95-104.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2016.10.012
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: MR (Mineralocorticoid Receptor) Induces Adipose Tissue Senescence and Mitochondrial Dysfunction Leading to Vascular Dysfunction in Obesity.

Lefranc, Clara / Friederich-Persson, Malou / Braud, Laura / Palacios-Ramirez, Roberto / Karlsson, Susanne / Boujardine, Nabiha / Motterlini, Roberto / Jaisser, Frederic / Nguyen Dinh Cat, Aurelie

Hypertension (Dallas, Tex. : 1979)

2019 Volume 73, Issue 2, Page(s) 458–468

Abstract: Adipose tissue (AT) senescence and mitochondrial dysfunction are associated with obesity. Studies in obese patients and animals demonstrate that the MR (mineralocorticoid receptor) contributes to obesity-associated cardiovascular complications through ... ...

Abstract	Adipose tissue (AT) senescence and mitochondrial dysfunction are associated with obesity. Studies in obese patients and animals demonstrate that the MR (mineralocorticoid receptor) contributes to obesity-associated cardiovascular complications through its specific role in AT. However, underlying mechanisms remain unclear. This study aims to elucidate whether MR regulates mitochondrial function in obesity, resulting in AT premature aging and vascular dysfunction. Obese (db/db) and lean (db/+) mice were treated with an MR antagonist or a specific mitochondria-targeted antioxidant. Mitochondrial and vascular functions were determined by respirometry and myography, respectively. Molecular mechanisms were probed by Western immunoblotting and real-time polymerase chain reaction in visceral AT and arteries and focused on senescence markers and redox-sensitive pathways. db/db mice displayed AT senescence with activation of the p53-p21 pathway and decreased SIRT (sirtuin) levels, as well as mitochondrial dysfunction. Furthermore, the beneficial anticontractile effects of perivascular AT were lost in db/db via ROCK (Rho kinase) activation. MR blockade prevented these effects. Thus, MR activation in obesity induces mitochondrial dysfunction and AT senescence and dysfunction, which consequently increases vascular contractility. In conclusion, our study identifies novel mechanistic insights involving MR, adipose mitochondria, and vascular function that may be of importance to develop new therapeutic strategies to limit obesity-associated cardiovascular complications.
MeSH term(s)	3T3-L1 Cells ; Adipose Tissue/physiology ; Animals ; Male ; Mice ; Mitochondria/metabolism ; Muscle, Smooth, Vascular/metabolism ; Obesity/physiopathology ; Reactive Oxygen Species/metabolism ; Receptors, Mineralocorticoid/physiology ; Sirtuin 1/physiology ; rho-Associated Kinases/physiology
Chemical Substances	Reactive Oxygen Species ; Receptors, Mineralocorticoid ; rho-Associated Kinases (EC 2.7.11.1) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2019-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.118.11873
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Zs.A 1488: Show issues

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