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  • 1.
    Gurung, Iman S.
    et al.
    Department of Physiology Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
    Medina-Gomez, Gema
    Metabolic Research Laboratories, Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom; Departamento de Bioquímica, Fisiología y Genética Molecular, Universidad Rey Juan Carlos, Madrid, Spain.
    Kis, Adrienn
    Metabolic Research Laboratories, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Baker, Michael
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, United Kingdom.
    Velagapudi, Vidya
    VTT Technical Research Centre of Finland, Espo, Finland.
    Neogi, Sudeshna Guha
    Genomics CoreLab, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Campbell, Mark
    Metabolic Research Laboratories, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Rodriguez-Cuenca, Sergio
    Metabolic Research Laboratories, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Lelliott, Christopher
    Metabolic Research Laboratories, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom; Department of Bioscience, CVGI IMED, AstraZeneca R and D, Mölndal, Sweden.
    McFarlane, Ian
    Genomics CoreLab, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Oresic, Matej
    Örebro University, School of Medical Sciences. VTT Technical Research Centre of Finland, Espo, Finland.
    Grace, Andrew A.
    Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
    Vidal-Puig, Antonio
    Metabolic Research Laboratories, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
    Huang, Christopher L-H.
    Department of Physiology Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, United Kingdom.
    Deletion of the metabolic transcriptional coactivator PGC1β induces cardiac arrhythmia2011In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 92, no 1, p. 29-38Article in journal (Refereed)
    Abstract [en]

    AIMS: Peroxisome proliferator-activated receptor-γ coactivators PGC1α and PGC1β modulate mitochondrial biogenesis and energy homeostasis. The function of these transcriptional coactivators is impaired in obesity, insulin resistance, and type 2 diabetes. We searched for transcriptomic, lipidomic, and electrophysiological alterations in PGC1β(-/-) hearts potentially associated with increased arrhythmic risk in metabolic diseases.

    METHODS AND RESULTS: Microarray analysis in mouse PGC1β(-/-) hearts confirmed down-regulation of genes related to oxidative phosphorylation and the electron transport chain and up-regulation of hypertrophy- and hypoxia-related genes. Lipidomic analysis showed increased levels of the pro-arrhythmic and pro-inflammatory lipid, lysophosphatidylcholine. PGC1β(-/-) mouse electrocardiograms showed irregular heartbeats and an increased incidence of polymorphic ventricular tachycardia following isoprenaline infusion. Langendorff-perfused PGC1β(-/-) hearts showed action potential alternans, early after-depolarizations, and ventricular tachycardia. PGC1β(-/-) ventricular myocytes showed oscillatory resting potentials, action potentials with early and delayed after-depolarizations, and burst firing during sustained current injection. They showed abnormal diastolic Ca(2+) transients, whose amplitude and frequency were increased by isoprenaline, and Ca(2+) currents with negatively shifted inactivation characteristics, with increased window currents despite unaltered levels of CACNA1C RNA transcripts. Inwardly and outward rectifying K(+) currents were all increased. Quantitiative RT-PCR demonstrated increased SCN5A, KCNA5, RYR2, and Ca(2+)-calmodulin dependent protein kinase II expression.

    CONCLUSION: PGC1β(-/-) hearts showed a lysophospholipid-induced cardiac lipotoxicity and impaired bioenergetics accompanied by an ion channel remodelling and altered Ca(2+) homeostasis, converging to produce a ventricular arrhythmic phenotype particularly during adrenergic stress. This could contribute to the increased cardiac mortality associated with both metabolic and cardiac disease attributable to lysophospholipid accumulation.

  • 2.
    Klarström-Engström, Kristin
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Skoglund, C.
    Linköping University, Linköping, Sweden.
    Kälvegren, Hanna
    Linköping University Hospital, Linköping, Sweden.
    Bengtsson, Torbjörn
    Örebro University, School of Medicine, Örebro University, Sweden.
    The role of platelets in inflammation at sites of infection: toll like receptor 2/1 mediated platelet adhesion on bacterial peptide-mimetic surfaces2012In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 93, p. S8-S8Article in journal (Other academic)
  • 3.
    Lönn, Johanna
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Clinical Medicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Hallström, J.
    Department of Clinical Medicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Bengtsson, Torbjörn
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Clinical Medicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    P. gingivalis-induced aggregation and ros production in whole blood is dependent on gingipains2012In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 93, p. S35-S35Article in journal (Other academic)
    Abstract [en]

    A large body of data accumulated over the past several years suggests that the periodontal pathogen Porphyromonas gingivalis is associated with cardiovascular disease. Circulating bacteria may contribute to atherogenesis by promoting CD11b/CD18-mediated interactions between neutrophils and platelets, causing reactive oxygen species (ROS) production and aggregation. We have previously demonstrated that P. gingivalis induces aggregation and ROS production in whole blood, and that the anti-inflammatory mediator lipoxin A4 (LXA4) inhibits these responses by modulating plateletneutrophil interaction through a down-regulation of the bacterium-induced surface expression of CD11b/CD18 on neutrophils, likely by inhibiting Rac2 and Cdc42 signaling pathways. Furthermore, P. gingivalis, unlike other periodontopathic bacteria, has been shown to trigger platelet aggregation, mainly through the interaction between bacterial gingipains and protease-activating receptors (PARs) on the platelets. Since platelet aggregation precedes thromboembolic events, this is an important pathogenic feature of the bacterium. The aim of this study was to investigate the effect of gingipains on P. gingivalis-induced cell activation in whole blood. Platelet/leukocyte aggregation and ROS production was examined by lumiaggregometry. This study shows that leupeptin, a protease inhibitor of gingipains, inhibits P. gingivalis-induced aggregation and ROS production in whole blood. Supernatants of bacteria suspensions induced no ROS-production, but an aggregatory response that was also inhibited by leupeptin. In conclusion, P. gingivalis-induced aggregation and ROS production in whole blood is mainly dependent on gingipains. However, since bacterial supernatants (containing soluble gingipains) stimulate only aggregation, this suggests that a gingipain/PAR-mediated mechanism in combination with phagocytosis of whole bacterium is a prerequisite for inducing a respiratory burst and an inflammatory response. These findings may contribute to new strategies in the prevention and treatment of periodontitis-induced inflammatory disorders, such as atherosclerosis.

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