Blood pressure regulation by CD4+ lymphocytes expressing choline acetyltransferase
A CD4 T-cell population expressing choline acetyltransferase is shown to contribute to blood pressure regulation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously...
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| Published in | Nature biotechnology Vol. 34; no. 10; pp. 1066 - 1071 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.10.2016
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | A CD4 T-cell population expressing choline acetyltransferase is shown to contribute to blood pressure regulation.
Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4
+
T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals
1
. Here we show that these CD4
+
CD44
hi
CD62L
lo
T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T
ChAT
). Mice lacking ChAT expression in CD4
+
cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT
ChAT
) decreased blood pressure when infused into mice. Co-incubation of JT
ChAT
and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T
ChAT
cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. |
|---|---|
| AbstractList | A CD4 T-cell population expressing choline acetyltransferase is shown to contribute to blood pressure regulation.
Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4
+
T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals
1
. Here we show that these CD4
+
CD44
hi
CD62L
lo
T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T
ChAT
). Mice lacking ChAT expression in CD4
+
cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT
ChAT
) decreased blood pressure when infused into mice. Co-incubation of JT
ChAT
and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T
ChAT
cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4(+) T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals(1). Here we show that these CD4(+)CD44(hi)CD62L(Io) T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T-ChAT). Mice lacking ChAT expression in CD4(+) cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT(ChAT)) decreased blood pressure when infused into mice. Co-incubation of JT(ChAT) and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T-ChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4 T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals. Here we show that these CD4 CD44 CD62L T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T ). Mice lacking ChAT expression in CD4 cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT ) decreased blood pressure when infused into mice. Co-incubation of JT and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been defined. We previously described that CD4 + T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals 1 . Here we show that these CD4 + CD44 high CD62L low T helper cells by gene expression are a distinct T cell population defined by ChAT (CD4 T ChAT ). Mice lacking ChAT expression in CD4 + cells have elevated arterial blood pressure and echocardiographic assessment consistent with increased vascular resistance as compared to littermate controls. Jurkat T cells overexpressing ChAT (JT ChAT ) decreased blood pressure when infused into mice. Co-incubation of JT ChAT increased endothelial cell levels of phosphorylated eNOS, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasodilator nitric oxide. The isolation and characterization of CD4 T ChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4+ T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals. Here we show that these CD4+CD44hiCD62Llo T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 TChAT). Mice lacking ChAT expression in CD4+ cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JTChAT) decreased blood pressure when infused into mice. Co-incubation of JTChAT and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 TChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation.Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4+ T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals. Here we show that these CD4+CD44hiCD62Llo T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 TChAT). Mice lacking ChAT expression in CD4+ cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JTChAT) decreased blood pressure when infused into mice. Co-incubation of JTChAT and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 TChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4+ T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals1. Here we show that these CD4+CD44hiCD62Llo T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 TChAT). Mice lacking ChAT expression in CD4+ cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JTChAT) decreased blood pressure when infused into mice. Co-incubation of JTChAT and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 TChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation. |
| Audience | Academic |
| Author | Andersson, Ulf Gregersen, Peter K Ahmed, Mohamed N Diamond, Betty Liu, Shu Fang Introini, Andrea Chavan, Sangeeta S Lövdahl, Cecilia Tracey, Kevin J Pavlov, Valentin A Olofsson, Peder S Arner, Anders Holodick, Nichol E Cox, Maureen A Steinberg, Benjamin E Broliden, Kristina Hanes, William M Sobbi, Roozbeh Miller, Edmund J Oswald, Michaela Mak, Tak W Szekeres, Ferenc Yang, Huan Rothstein, Thomas L Backx, Peter H |
| AuthorAffiliation | 13 Department of Biology, York University, Toronto, Ontario, Canada 6 Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, NY, USA 9 Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, Manhasset, NY, USA 7 Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden 8 Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden 3 The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada 4 Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada 12 School of Health and Education, University of Skövde, Skövde, Sweden 5 Center for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, NY, USA 1 Center for Bioelectronic Medicine, Department of Medicine, Solna, Karolinska |
| AuthorAffiliation_xml | – name: 1 Center for Bioelectronic Medicine, Department of Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden – name: 13 Department of Biology, York University, Toronto, Ontario, Canada – name: 10 Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden – name: 3 The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada – name: 12 School of Health and Education, University of Skövde, Skövde, Sweden – name: 2 Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, NY, USA – name: 11 The Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, USA – name: 7 Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden – name: 6 Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, NY, USA – name: 8 Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden – name: 5 Center for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, NY, USA – name: 9 Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, Manhasset, NY, USA – name: 4 Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada |
| Author_xml | – sequence: 1 givenname: Peder S surname: Olofsson fullname: Olofsson, Peder S email: peder.olofsson@ki.se organization: Department of Medicine, Center for Bioelectronic Medicine, Center for Molecular Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Laboratory of Biomedical Science, The Feinstein Institute for Medical Research – sequence: 2 givenname: Benjamin E surname: Steinberg fullname: Steinberg, Benjamin E organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, The Campbell Family Institute for Breast Cancer Research, University Health Network – sequence: 3 givenname: Roozbeh surname: Sobbi fullname: Sobbi, Roozbeh organization: Division of Cardiology, Peter Munk Cardiac Centre, University Health Network – sequence: 4 givenname: Maureen A surname: Cox fullname: Cox, Maureen A organization: The Campbell Family Institute for Breast Cancer Research, University Health Network – sequence: 5 givenname: Mohamed N surname: Ahmed fullname: Ahmed, Mohamed N organization: Center for Heart and Lung Research, The Feinstein Institute for Medical Research – sequence: 6 givenname: Michaela surname: Oswald fullname: Oswald, Michaela organization: Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research – sequence: 7 givenname: Ferenc surname: Szekeres fullname: Szekeres, Ferenc organization: Department of Physiology and Pharmacology, Karolinska Institutet, School of Health and Education, University of Skövde – sequence: 8 givenname: William M surname: Hanes fullname: Hanes, William M organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research – sequence: 9 givenname: Andrea orcidid: 0000-0002-9929-8964 surname: Introini fullname: Introini, Andrea organization: Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital – sequence: 10 givenname: Shu Fang surname: Liu fullname: Liu, Shu Fang organization: Center for Heart and Lung Research, The Feinstein Institute for Medical Research – sequence: 11 givenname: Nichol E surname: Holodick fullname: Holodick, Nichol E organization: Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research – sequence: 12 givenname: Thomas L surname: Rothstein fullname: Rothstein, Thomas L organization: Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research – sequence: 13 givenname: Cecilia surname: Lövdahl fullname: Lövdahl, Cecilia organization: Department of Physiology and Pharmacology, Karolinska Institutet – sequence: 14 givenname: Sangeeta S surname: Chavan fullname: Chavan, Sangeeta S organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research – sequence: 15 givenname: Huan surname: Yang fullname: Yang, Huan organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research – sequence: 16 givenname: Valentin A surname: Pavlov fullname: Pavlov, Valentin A organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research – sequence: 17 givenname: Kristina orcidid: 0000-0003-2224-7664 surname: Broliden fullname: Broliden, Kristina organization: Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital – sequence: 18 givenname: Ulf surname: Andersson fullname: Andersson, Ulf organization: Department of Women's and Children's Health, Karolinska Institutet – sequence: 19 givenname: Betty orcidid: 0000-0002-3250-3804 surname: Diamond fullname: Diamond, Betty organization: The Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research – sequence: 20 givenname: Edmund J orcidid: 0000-0002-2131-0054 surname: Miller fullname: Miller, Edmund J organization: Center for Heart and Lung Research, The Feinstein Institute for Medical Research – sequence: 21 givenname: Anders surname: Arner fullname: Arner, Anders organization: Department of Physiology and Pharmacology, Karolinska Institutet – sequence: 22 givenname: Peter K surname: Gregersen fullname: Gregersen, Peter K organization: Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research – sequence: 23 givenname: Peter H surname: Backx fullname: Backx, Peter H organization: Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Department of Biology, York University – sequence: 24 givenname: Tak W surname: Mak fullname: Mak, Tak W organization: The Campbell Family Institute for Breast Cancer Research, University Health Network – sequence: 25 givenname: Kevin J surname: Tracey fullname: Tracey, Kevin J organization: Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Department of Women's and Children's Health, Karolinska Institutet |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27617738$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-13115$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:134468317$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Copyright | Springer Nature America, Inc. 2016 COPYRIGHT 2016 Nature Publishing Group Copyright Nature Publishing Group Oct 2016 |
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| DOI | 10.1038/nbt.3663 |
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| Snippet | A CD4 T-cell population expressing choline acetyltransferase is shown to contribute to blood pressure regulation.
Blood pressure regulation is known to be... Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not... |
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| SubjectTerms | 38 631/250/1619/554/1898 631/378/2607 631/443/592/75/243 631/80/304 64/110 692/308/1426 96/106 Age and Ageing Agriculture Animals Bioinformatics Biomedical Engineering/Biotechnology Biomedicine Biotechnology Blood pressure Blood Pressure - physiology CD4-positive T cells CD4-Positive T-Lymphocytes - physiology Cells, Cultured Choline O-Acetyltransferase - metabolism Control Enzymes Experimental models of disease Feedback, Physiological - physiology Female Health aspects Hemostasis - physiology Homeostasis Hypertension Immune system letter Life Sciences Lymphocytes Male Mechanisms of disease Mice Mice, Inbred C57BL Neuro–vascular interactions Nitrates Nitric oxide Nitrites Transferases Äldre och åldrande |
| Title | Blood pressure regulation by CD4+ lymphocytes expressing choline acetyltransferase |
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