The Role of Reactive Oxygen Species in β-Adrenergic Signaling in Cardiomyocytes from Mice with the Metabolic Syndrome
The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased product...
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| Published in | PloS one Vol. 11; no. 12; p. e0167090 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.12.2016
Public Library of Science (PLoS) |
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| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0167090 |
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| Abstract | The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels. |
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| AbstractList | The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels. The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels.The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels. The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca 2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca 2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels. The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca 2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca 2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels. |
| Author | Jardemark, Kent Zhang, Shi-Jin Zong, Mei Westerblad, Håkan Yamada, Takashi Andersson, Daniel C. Fauconnier, Jeremy Katz, Abram Sinclair, Jon Lanner, Johanna T. Llano-Diez, Monica |
| AuthorAffiliation | Universidad Pablo de Olavide, SPAIN 1 Karolinska Institutet, Department of Physiology & Pharmacology, Stockholm, Sweden 3 Karolinska Institutet, Department of Medicine, Stockholm, Sweden 2 Karolinska University Hospital, Rheumatology unit, CMM, Stockholm Sweden |
| AuthorAffiliation_xml | – name: 3 Karolinska Institutet, Department of Medicine, Stockholm, Sweden – name: 1 Karolinska Institutet, Department of Physiology & Pharmacology, Stockholm, Sweden – name: 2 Karolinska University Hospital, Rheumatology unit, CMM, Stockholm Sweden – name: Universidad Pablo de Olavide, SPAIN |
| Author_xml | – sequence: 1 givenname: Monica surname: Llano-Diez fullname: Llano-Diez, Monica – sequence: 2 givenname: Jon surname: Sinclair fullname: Sinclair, Jon – sequence: 3 givenname: Takashi surname: Yamada fullname: Yamada, Takashi – sequence: 4 givenname: Mei surname: Zong fullname: Zong, Mei – sequence: 5 givenname: Jeremy surname: Fauconnier fullname: Fauconnier, Jeremy – sequence: 6 givenname: Shi-Jin surname: Zhang fullname: Zhang, Shi-Jin – sequence: 7 givenname: Abram surname: Katz fullname: Katz, Abram – sequence: 8 givenname: Kent surname: Jardemark fullname: Jardemark, Kent – sequence: 9 givenname: Håkan surname: Westerblad fullname: Westerblad, Håkan – sequence: 10 givenname: Daniel C. surname: Andersson fullname: Andersson, Daniel C. – sequence: 11 givenname: Johanna T. orcidid: 0000-0002-1222-9473 surname: Lanner fullname: Lanner, Johanna T. |
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| Copyright | 2016 Llano-Diez et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Distributed under a Creative Commons Attribution 4.0 International License 2016 Llano-Diez et al 2016 Llano-Diez et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Current address: University of Montpellier, U1046 INSERM, Montpellier, France Current address: Ariel University, Department of Physical Therapy, School of Health Sciences, Ariel, Israel Competing Interests: The authors have declared that no competing interests exist. Current address: Sapporo Medical University, Graduate School of Health Sciences, Sapporo, Japan Conceptualization: MLD HW DCA JTL.Formal analysis: MLD JS AK KJ HW DCA JTL.Funding acquisition: HW JTL.Investigation: MLD JS TY MZ JF SJZ AK KJ DCA JTL.Methodology: MLD JS TY MZ JF SJZ AK KJ HW DCA JTL.Project administration: JTL.Resources: HW DCA JTL.Supervision: HW DCA JTL.Validation: MLD JS HW DCA JTL.Visualization: MLD HW DCA JTL.Writing – original draft: MLD DCA JTL.Writing – review & editing: MLD JS TY MZ JF SJZ AK KJ HW DCA JTL. |
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| SubjectTerms | Adrenergic beta-Agonists - pharmacology Adrenergic transmission Animal models Animals Antioxidants Biochemistry Biochemistry, Molecular Biology Biology and Life Sciences Calcium (intracellular) Calcium (mitochondrial) Calcium - metabolism Calcium signalling Cardiology and cardiovascular system Cardiomyocytes Cardiomyopathies - etiology Cardiomyopathies - metabolism Cardiomyopathies - pathology Cardiovascular diseases Cellular manufacture Confocal microscopy Diabetes Diet Diet, High-Fat - adverse effects Electric Stimulation Experiments Fluorescence Fluorescent dyes Fluorescent indicators Gene expression Health sciences Heart Heart diseases Heart failure High fat diet Human health and pathology Hydrogen Peroxide - pharmacology Hyperactivity Immunofluorescence Insulin resistance Isoproterenol - pharmacology Kinases Life Sciences Male Medicine and Health Sciences Metabolic disorders Metabolic syndrome Metabolic Syndrome - etiology Metabolic Syndrome - metabolism Metabolic Syndrome - pathology Mice Mice, Inbred C57BL Microscopy Mitochondria Mitochondria - drug effects Mitochondria - metabolism Muscle contraction Musculoskeletal system Myocardial Contraction - drug effects Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Nervous system Obesity - etiology Obesity - metabolism Obesity - pathology Organ Culture Techniques Oxidative stress Oxygen Pharmacology Physiology Primary Cell Culture Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Adrenergic, beta - metabolism Research and Analysis Methods Rodents Signal Transduction Stimulation Sympathetic nervous system |
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| Title | The Role of Reactive Oxygen Species in β-Adrenergic Signaling in Cardiomyocytes from Mice with the Metabolic Syndrome |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/27907040 https://www.proquest.com/docview/1845246744 https://www.proquest.com/docview/1845818680 https://hal.umontpellier.fr/hal-01800533 https://pubmed.ncbi.nlm.nih.gov/PMC5131978 http://kipublications.ki.se/Default.aspx?queryparsed=id:134791519 https://doaj.org/article/2afc145d9b3f4b469f213fe4608f64ef http://dx.doi.org/10.1371/journal.pone.0167090 |
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