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  • 1.
    Cao, Yihai
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Karolinska Institute, Sweden .
    Angiogenesis and Vascular Functions in Modulation of Obesity, Adipose Metabolism, and Insulin Sensitivity2013In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 18, no 4, p. 478-489Article, review/survey (Refereed)
    Abstract [en]

    White and brown adipose tissues are hypervascularized and the adipose vasculature displays phenotypic and functional plasticity to coordinate with metabolic demands of adipocytes. Blood vessels not only supply nutrients and oxygen to nourish adipocytes, they also serve as a cellular reservoir to provide adipose precursor and stem cells that control adipose tissue mass and function. Multiple signaling molecules modulate the complex interplay between the vascular system and the adipocytes. Understanding fundamental mechanisms by which angiogenesis and vasculatures modulate adipocyte functions may provide new therapeutic options for treatment of obesity and metabolic disorders by targeting the adipose vasculature.

  • 2.
    Dong, Mei
    et al.
    Shandong University, Peoples R China .
    Yang, Xiaoyan
    Shandong University, Peoples R China .
    Lim, Sharon
    Karolinska Institute, Sweden .
    Cao, Ziquan
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences.
    Honek, Jennifer
    Karolinska Institute, Sweden .
    Lu, Huixia
    Shandong University, Peoples R China .
    Zhang, Cheng
    Shandong University, Peoples R China .
    Seki, Takahiro
    Karolinska Institute, Sweden .
    Hosaka, Kayoko
    Karolinska Institute, Sweden .
    Wahlberg, Eric
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Yang, Jianmin
    Shandong University, Peoples R China .
    Zhang, Lei
    Shandong University, Peoples R China .
    Länne, Toste
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Sun, Baocun
    Tianjin Medical University, Peoples R China .
    Li, Xuri
    Sun Yat Sen University, Peoples R China .
    Liu, Yizhi
    Sun Yat Sen University, Peoples R China .
    Zhang, Yun
    Shandong University, Peoples R China .
    Cao, Yihai
    Karolinska Institute, Sweden .
    Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis2013In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 18, no 1, p. 118-129Article in journal (Refereed)
    Abstract [en]

    Molecular mechanisms underlying the cold-associated high cardiovascular risk remain unknown. Here, we show that the cold-triggered food-intake-independent lipolysis significantly increased plasma levels of small low-density lipoprotein (LDL) remnants, leading to accelerated development of atherosclerotic lesions in mice. In two genetic mouse knockout models (apolipoprotein E-/- [ApoE(-/-)] and LDL receptor(-/-) [Ldlr(-/-)] mice), persistent cold exposure stimulated atherosclerotic plaque growth by increasing lipid deposition. Furthermore, marked increase of inflammatory cells and plaque-associated microvessels were detected in the cold-acclimated ApoE(-/-) and Ldlr(-/-) mice, leading to plaque instability. Deletion of uncoupling protein 1 (UCP1), a key mitochondrial protein involved in thermogenesis in brown adipose tissue (BAT), in the ApoE(-/-) strain completely protected mice from the cold-induced atherosclerotic lesions. Cold acclimation markedly reduced plasma levels of adiponectin, and systemic delivery of adiponectin protected ApoE(-/-) mice from plaque development. These findings provide mechanistic insights on low-temperature-associated cardiovascular risks.

  • 3.
    Holleboom, Adriaan G
    et al.
    Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Karlsson, Helen
    Linköping University, Department of Clinical and Experimental Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Occupational and Environmental Medicine Centre.
    Lin, Ruei-Shiuan
    Section on Biological Chemistry, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
    Beres, Thomas M
    Section on Biological Chemistry, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
    Sierts, Jeroen A
    Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Herman, Daniel S
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
    Stroes, Erik S G
    Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Aerts, Johannes M
    Department of Medical Biochemistry, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Kastelein, John J P
    Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Motazacker, Mohammad M
    Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Dallinga-Thie, Geesje M
    Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Levels, Johannes H M
    Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Zwinderman, Aeilko H
    Department of Clinical Epidemiology, Biostatistics, and Bioinformatics, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Seidman, Jonathan G
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
    Seidman, Christine E
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
    Ljunggren, Stefan
    Linköping University, Department of Clinical and Experimental Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences.
    Lefeber, Dirk J
    Department of Neurology, Radboud University Nijmegen Medical Center, Nijmegen 6525GA, The Netherlands.
    Morava, Eva
    Institute for Genetic and Metabolic Disease, Radboud University Nijmegen Medical Center, Nijmegen 6525GA, The Netherlands.
    Wevers, Ron A
    Department of Laboratory Medicine, Radboud University Nijmegen Medical Center, Nijmegen 6525GA, The Netherlands.
    Fritz, Timothy A
    Food and Drug Administration, Rockville, MD 20852, USA.
    Tabak, Lawrence A
    Section on Biological Chemistry, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
    Lindahl, Mats
    Linköping University, Department of Clinical and Experimental Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences.
    Hovingh, G Kees
    Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Kuivenhoven, Jan Albert
    Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands.
    Heterozygosity for a Loss-of-Function Mutation in GALNT2 Improves Plasma Triglyceride Clearance in Man2011In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 14, no 6, p. 811-8Article in journal (Refereed)
    Abstract [en]

    Genome-wide association studies have identified GALNT2 as a candidate gene in lipid metabolism, but it is not known how the encoded enzyme ppGalNAc-T2, which contributes to the initiation of mucin-type O-linked glycosylation, mediates this effect. In two probands with elevated plasma high-density lipoprotein cholesterol and reduced triglycerides, we identified a mutation in GALNT2. It is shown that carriers have improved postprandial triglyceride clearance, which is likely attributable to attenuated glycosylation of apolipoprotein (apo) C-III, as observed in their plasma. This protein inhibits lipoprotein lipase (LPL), which hydrolyses plasma triglycerides. We show that an apoC-III-based peptide is a substrate for ppGalNAc-T2 while its glycosylation by the mutant enzyme is impaired. In addition, neuraminidase treatment of apoC-III which removes the sialic acids from its glycan chain decreases its potential to inhibit LPL. Combined, these data suggest that ppGalNAc-T2 can affect lipid metabolism through apoC-III glycosylation, thereby establishing GALNT2 as a lipid-modifying gene.

  • 4.
    Oishi, Yumiko
    et al.
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA // Department of Cellular and Molecular Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
    Spann, Nathanael J
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Link, Verena M
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA // Department II, Faculty of Biology, Ludwig-Maximilians Universität München, Planegg-Martinsried 82152, Germany.
    Muse, Evan D
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA // Scripps Translational Science Institute, La Jolla, CA 92037, USA.
    Strid, Tobias
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Edillor, Chantle
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Kolar, Matthew J
    Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
    Matsuzaka, Takashi
    Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, Graduate School of Comprehensive Human Sciences, International Institute for Integrative Sleep Medicine (WPI-IIIS), and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki Prefecture 305-8571, Japan.
    Hayakawa, Sumio
    Department of Cellular and Molecular Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
    Tao, Jenhan
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Kaikkonen, Minna U
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA // Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
    Carlin, Aaron F
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Lam, Michael T
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    Manabe, Ichiro
    Department of Aging Research, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
    Shimano, Hitoshi
    Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, Graduate School of Comprehensive Human Sciences, International Institute for Integrative Sleep Medicine (WPI-IIIS), and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki Prefecture 305-8571, Japan.
    Saghatelian, Alan
    Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
    Glass, Christopher K
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
    SREBP1 Contributes to Resolution of Pro-inflammatory TLR4 Signaling by Reprogramming Fatty Acid Metabolism2017In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 25, no 2, p. 412-427, article id S1550-4131(16)30588-5Article in journal (Refereed)
    Abstract [en]

    Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators. Unexpectedly, rather than requiring LXRs, this late program of anti-inflammatory fatty acid biosynthesis is dependent on SREBP1 and results in the uncoupling of NFκB binding from gene activation. In contrast to previously identified roles of SREBP1 in promoting production of IL1β during the induction phase of inflammation, these studies provide evidence that SREBP1 also contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism.

1 - 4 of 4
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