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  • 1
    Online Resource
    Online Resource
    Hypercholesterolemia Induces Oxidant Stress That Accelerates the Ageing of Hematopoietic Stem Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Journal of the American Heart Association Vol. 3, No. 1 ( 2014-01-27)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 3, No. 1 ( 2014-01-27)
    Abstract: Clinical studies suggest that hypercholesterolemia may cause ageing in hematopoietic stem cells ( HSC s) because ageing‐associated alterations were found in peripheral blood cells and their bone marrow residing precursors in patients with advanced atherosclerosis. We hypothesized that hypercholesterolemia induces oxidant stress in hematopoietic stems cells that accelerates their ageing. Methods and Results Here we show that HSC s from ApoE −/− mice, as well as HSC s from C57Bl/6 mice fed a high cholesterol diet ( HCD ) accumulated ox LDL and had greater ROS levels. In accordance, the expression pattern of the genes involved in ROS metabolism changed significantly in HSC s from ApoE −/− mice. Hypercholesterolemia caused a significant reduction in phenotypically defined long‐term HSC compartment, telomere length, and repopulation capacity of KTLS cells, indicating accelerated ageing in these cells. Gene array analysis suggested abnormal cell cycle status, and the key cell cycle regulators including p19 ARF , p27 Kip1 and p21 Waf1 were upregulated in KTLS cells from hypercholesterolemic mice. These effects were p38‐dependent and reversed in vivo by treatment of hypercholesterolemic mice with antioxidant N ‐acetylcysteine. The oxidant stress also caused aberrant expression of Notch1 that caused loss of quiescence and proliferation leading to the expansion of KTLS compartment in hypercholesterolemic mice. Conclusion Taken together, we provide evidence that hypercholesterolemia can cause oxidant stress that accelerates the ageing and impairs the reconstitution capacity of HSC s.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.113.000241
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2653953-6
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  • 2
    Online Resource
    Online Resource
    Les stratégies thérapeutiques médicamenteuses et non médicamenteuses de l’aide à l’arrêt du tabac
    Elsevier BV ; 2003
    In:  Therapies Vol. 58, No. 6 ( 2003-11), p. 479-497
    Details
    In: Therapies, Elsevier BV, Vol. 58, No. 6 ( 2003-11), p. 479-497
    Type of Medium: Online Resource
    ISSN: 0040-5957
    URL: Article
    DOI: 10.2515/therapie:2003080
    Language: French
    Publisher: Elsevier BV
    Publication Date: 2003
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  • 3
    Online Resource
    Online Resource
    Abstract 634: Hypercholesterolemia Increases the Incidence of Colorectal Neoplasia by Impairing Hematopoietic Stem Cell Differentiation Towards Nkt and γδ T Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 35, No. suppl_1 ( 2015-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. suppl_1 ( 2015-05)
    Abstract: Rationale: Hypercholesterolemia, a co-morbidity of obesity, is one of the most common diet-related metabolic disorders and is an independent risk factor for colorectal neoplasia. As yet, no generalizable mechanism has been described to show how hypercholesterolemia increases the risk of cancer especially that of colorectal neoplasia. Objective: We hypothesized that hypercholesterolemia impaired the differentiation of hematopoietic stem cells (HSCs) toward the cellular components critical to immunosurveillance against colorectal neoplasia. Identifying the mechanisms by which hypercholesterolemia affects HSC differentiation may provide clues to understanding how hypercholesterolemia increases all-cause mortality and especially that of colorectal cancer in divergent clinical studies. Methods and Results: Two different hypercholesterolemic mice were applied in the study, including ApoE-/- mouse and high cholesterol diet fed WT mouse. Colorectal neoplasia was induced by IP injection of AOM. The incidence of colorectal neoplasia was significantly higher in these hypercholesterolemic mice. FACS analysis showed that NKT and γδT cells were significantly fewer in the thymus and colon of hypercholesterolemic mice. The infiltration of NKT and γδT cells in tumors isolated from hypercholesterolemic mice was attenuated. In agreement, in vitro differentiation assay demonstrated that the differentiation capacity of HSCs towards NKT and γδT cells was significantly impaired in the groups isolated from hypercholesterolemic mice. The deficiency in NKT or γδT cells increased the incidence of AOM-induced colorectal neoplasia. Conclusion: NKT and γδT cells are critical cellular components in the immnuosurveillance against colorectal neoplasia. Hypercholesterolemia increases the incidence of colorectal neoplasia by impairing the differentiation of HSCs towards NKT and γδT cells.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.35.suppl_1.634
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1494427-3
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  • 4
    Online Resource
    Online Resource
    Abstract 120: Reversal of Nox 4-Induced Oxidative Stress in Type 2 Diabetic Mesenchymal Stem Cells Restores Their Capacity to Augment Postischemic Neovascularization in db/db Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 32, No. suppl_1 ( 2012-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. suppl_1 ( 2012-05)
    Abstract: Rationale: We have recently shown that experimental type 2 diabetes (db/db mouse) restricts mesenchymal stem cell’ (MSCs) differentiation capacity through a hyperinsulinemia-dependent induction of Nox 4 expression that promotes adipocytic and inhibits endothelial cell differentiation both in vitro and in vivo. We also showed that transplantation of type 2 diabetic MSCs into wild type (WT) recipients reduced post-ischemic neovascularization significantly below that of WT recipients receiving WT MSCs. Objective: This study tested the hypothesis that pretreatment of db/db MSCs with siRNA Nox4 prior to their transplantation and infusion 24 hrs after the induction of hindlimb ischemia restores their differentiation capacity in vivo and rescues their impaired capacity to promote neovascularization in wild type mice. Methods and Results: To reverse oxidative stress in db/db MSCs, we knockdown NOX 4 expression by a siRNA under in vitro conditions. In vitro inhibition of Nox 4 expression of db/db MSCs significantly increased their differentiation capacity towards endothelial cells and reduced their propensity to differentiate into adipocytes. Db/db MSCs also showed significantly increased tubular formation ability after Nox 4 knockdown. We transplanted NOX 4 siRNA transduced db/db MSCs into WT recipients 24 hours after induction of hindlimb ischemia. Blood flow recovery was measured at different time points by laser Doppler scanning. Reversal of oxidative stress in db/db MSCs by pretreatment with Nox4 siRNA prior to transplantation reversed their impaired capacity to augment post-ischemic neovascularization as evidenced by blood flow recovery that increased to that of WT mice. In addition, knockdown of NOX 4 expression in db/db MSCs also increased collateral artery diameter and capillary density by 50%. Conclusions: Pretreatment of db/db MSCs with siRNA against Nox 4 significantly increased their differentiation capacity towards endothelial cells rather than adipocytes and also their capacity to augment neovascularization after induction of hindlimb ischemia. Reversal of MSC oxidant stress induced by type 2 diabetes might permit greater leverage of the therapeutic potential of MSC transplantation to treat cardiovascular diseases.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.32.suppl_1.A120
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1494427-3
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  • 5
    Online Resource
    Online Resource
    Type 2 Diabetes Restricts Multipotency of Mesenchymal Stem Cells and Impairs Their Capacity to Augment Postischemic Neovascularization in db/db Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Journal of the American Heart Association Vol. 1, No. 6 ( 2012-11-29)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 1, No. 6 ( 2012-11-29)
    Abstract: This study tested the hypothesis that type 2 diabetes restricts multipotency of db/db mesenchymal stem cells ( MSC s), promotes their terminal differentiation into adipocytes rather than endothelial cells, thereby promotes adipocytic infiltration into ischemic muscles, and reduces their capacity to participate in postischemic neovascularization. Methods and Results To test this hypothesis, we transplanted MSC s from db/db or wild‐type ( WT ) mice into WT recipients after induction of hind limb ischemia. WT recipients of db/db MSC s demonstrated adipocyte infiltration of ischemic muscle and impaired neovascularization; WT recipients of WT MSC s showed no intramuscular adipocyte infiltration and had significantly enhanced neovascularization ( P 〈 0.05; n=6). Confocal microscopy showed that the percentage of MSC s that differentiated into an adipocyte phenotype was greater and into an endothelial cell was less in WT recipients transplanted with db/db MSC s than those transplanted with WT MSC s ( P 〈 0.05; n=6). In vitro, db/db MSC s exhibited greater oxidant stress, greater adipocyte differentiation, and less endothelial differentiation than WT MSC s, and these differences were reversed by treatment with N ‐acetylcysteine or Nox4 siRNA ( P 〈 0.05; n=6). Insulin increased Nox4 expression, oxidant stress, and adipocyte differentiation in WT MSC s, and these insulin‐induced effects were reversed by Nox4 siRNA ( P 〈 0.05; n=6). Reversal of db/db MSC oxidant stress by in vivo pretreatment with Nox4 siRNA before transplantation reversed their impaired capacity to augment postischemic neovascularization. Conclusions Type 2 diabetes–induced oxidant stress restricts the multipotency of MSC s and impairs their capacity to increase blood flow recovery after the induction of hind‐limb ischemia. Reversal of MSC oxidant stress might permit greater leverage of the therapeutic potential of MSC transplantation in the setting of diabetes.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.112.002238
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2653953-6
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  • 6
    Online Resource
    Online Resource
    Large effects of tiny structural changes on the cluster formation process in model colloidal fluids: an integral equation study
    American Institute of Mathematical Sciences (AIMS) ; 2020
    In:  AIMS Materials Science Vol. 7, No. 2 ( 2020), p. 170-181
    Details
    In: AIMS Materials Science, American Institute of Mathematical Sciences (AIMS), Vol. 7, No. 2 ( 2020), p. 170-181
    Type of Medium: Online Resource
    ISSN: 2372-0484
    URL: Article
    DOI: 10.3934/matersci.2020.2.170
    Language: English
    Publisher: American Institute of Mathematical Sciences (AIMS)
    Publication Date: 2020
    detail.hit.zdb_id: 2777112-X
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  • 7
    Online Resource
    Online Resource
    Hypercholesterolemia Increases Colorectal Cancer Incidence by Reducing Production of NKT and γδ T Cells from Hematopoietic Stem Cells
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 9 ( 2017-05-01), p. 2351-2362
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 9 ( 2017-05-01), p. 2351-2362
    Abstract: Obesity will soon surpass smoking as the most preventable cause of cancer. Hypercholesterolemia, a common comorbidity of obesity, has been shown to increase cancer risk, especially colorectal cancer. However, the mechanism by which hypercholesterolemia or any metabolic disorder increases cancer risk remains unknown. In this study, we show that hypercholesterolemia increases the incidence and pathologic severity of colorectal neoplasia in two independent mouse models. Hypocholesterolemia induced an oxidant stress–dependent increase in miR101c, which downregulated Tet1 in hematopoietic stem cells (HSC), resulting in reduced expression of genes critical to natural killer T cell (NKT) and γδ T-cell differentiation. These effects reduced the number and function of terminally differentiated NKT and γδ T cells in the thymus, the colon submucosa, and during early tumorigenesis. These results suggest a novel mechanism by which a metabolic disorder induces epigenetic changes to reduce lineage priming of HSC toward immune cells, thereby compromising immunosurveillance against cancer. Cancer Res; 77(9); 2351–62. ©2017 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-16-1916
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
    Online Resource
    Online Resource
    Oxidized Low-Density Lipoprotein Induces Apoptosis in Endothelial Progenitor Cells by Inactivating the Phosphoinositide 3-Kinase/Akt Pathway
    S. Karger AG ; 2010
    In:  Journal of Vascular Research Vol. 47, No. 6 ( 2010), p. 519-530
    Details
    In: Journal of Vascular Research, S. Karger AG, Vol. 47, No. 6 ( 2010), p. 519-530
    Abstract: We tested the hypothesis that oxidized low-density lipoprotein (oxLDL)-induced inactivation of Akt within endothelial progenitor cells (EPCs) is mediated at the level of Phosphoinositide 3-kinase (PI3K), specifically by nitrosylation of the p85 subunit of PI3K, and that this action is critical in provoking oxLDL-induced EPC apoptosis. Hypercholesterolemic ApoE null mice had a significant reduction of the phosphorylated Akt (p-Akt)/Akt ratio in EPCs, as well as a greater percentage of apoptosis in these cells than EPCs isolated from wild-type (WT) C57Bl/6 mice. EPCs were isolated from WT spleen and exposed to oxLDL in vitro. oxLDL increased O 〈 sub 〉 2 〈 /sub 〉 〈 sup 〉 – 〈 /sup 〉 and H 〈 sub 〉 2 〈 /sub 〉 O 〈 sub 〉 2 〈 /sub 〉 in these cells and induced a dose- and time-dependent reduction in the p-Akt/Akt ratio and increase in EPC apoptosis. These effects were significantly reduced by the antioxidants superoxide dismutase, 〈 i 〉 L 〈 /i 〉 -NAME, epicatechin and FeTPPs. oxLDL also induced nitrosylation of the p85 subunit of PI3K and subsequent dissociation of the p85 and p110 subunits, an effect significantly reduced by all the antioxidant agents tested. EPC transfection with a constitutively active Akt isoform (Ad-myrAkt) significantly reduced oxLDL-induced apoptosis of WT EPCs. The present findings indicate that oxLDL disrupts the PI3K/Akt signaling pathway at the level of p85 in EPCs. This dysfunction can be reversed by ex vivo antioxidant therapy.
    Type of Medium: Online Resource
    ISSN: 1018-1172 , 1423-0135
    URL: Article
    DOI: 10.1159/000313879
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1482726-8
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  • 9
    Online Resource
    Online Resource
    Inhibition of p38 Mitogen-Activated Protein Kinase Enhances the Apoptosis Induced by Oxidized Low-Density Lipoprotein in Endothelial Progenitor Cells
    S. Karger AG ; 2015
    In:  Journal of Vascular Research Vol. 52, No. 6 ( 2015), p. 361-371
    Details
    In: Journal of Vascular Research, S. Karger AG, Vol. 52, No. 6 ( 2015), p. 361-371
    Abstract: Oxidized low-density lipoprotein (oxLDL) is an important risk factor in the development of atherosclerosis. oxLDL has been shown to decrease endothelial progenitor cell (EPC) number by inducing apoptosis. p38 mitogen-activated protein kinase (MAPK) was shown to be activated by oxLDL and participated in the regulation of EPC number and function. However, the role of p38 remains unknown. Here, we show that oxLDL-induced p38 phosphorylation in EPCs is time and dose dependent. Treatment with antioxidant N-acetyl cysteine restored oxLDL-induced p38 phosphorylation to basal levels. LOX-1-blocking antibody also significantly decreased oxLDL-induced p38 phosphorylation. Interestingly, TUNEL staining showed that pretreatment with the p38 inhibitor SB203580 further increased oxLDL-induced apoptosis in EPCs. In accordance with these findings, pretreatment with SB203580 further attenuated Akt phosphorylation in EPCs challenged with oxLDL, indicating an interaction between Akt and p38 MAPK pathways. In agreement, inhibition of p38 MAPK further attenuated Akt phosphorylation and increased apoptosis in EPCs isolated from hypercholesterolemic ApoE-/- mice. In conclusion, p38 MAPK serves as an anti-apoptotic pathway by supporting Akt activity when EPCs are challenged with oxLDL.
    Type of Medium: Online Resource
    ISSN: 1018-1172 , 1423-0135
    URL: Article
    DOI: 10.1159/000443889
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482726-8
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  • 10
    Online Resource
    Online Resource
    PP44. Determinants of Hospital Disposition after Lower Extremity Bypass Surgery
    Elsevier BV ; 2009
    In:  Journal of Vascular Surgery Vol. 49, No. 5 ( 2009-05), p. S27-
    Details
    In: Journal of Vascular Surgery, Elsevier BV, Vol. 49, No. 5 ( 2009-05), p. S27-
    Type of Medium: Online Resource
    ISSN: 0741-5214
    URL: Article
    DOI: 10.1016/j.jvs.2009.02.074
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 1492043-8
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