Activated Platelets Induce Endothelial Cell Inflammatory Response in Psoriasis via COX-1
Patients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular dysfunction in cardiovascular disease and represent therapeutic targets in cardiovascular prevention. The object of this study was to define the...
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| Vydáno v: | Arteriosclerosis, thrombosis, and vascular biology Ročník 40; číslo 5; s. 1340 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
01.05.2020
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| ISSN: | 1524-4636, 1524-4636 |
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| Abstract | Patients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular dysfunction in cardiovascular disease and represent therapeutic targets in cardiovascular prevention. The object of this study was to define the platelet phenotype and effector cell properties on vascular health in psoriasis and evaluate whether aspirin modulates the platelet-induced phenotype. Approach and Results: Platelets from psoriasis patients (n=45) exhibited increased platelet activation (relative to age- and gender-matched controls, n=18), which correlated with psoriasis skin severity. Isolated platelets from psoriasis patients demonstrated a 2- to 3-fold (
<0.01) increased adhesion to human aortic endothelial cells and induced proinflammatory transcriptional changes, including upregulation of
(interleukin 8),
, and Cox (cyclooxygenase)-2 Platelet RNA sequencing revealed an interferon signature and elevated expression of
, which correlated with psoriasis disease severity (
=0.83,
=0.01). In a randomized trial of patients with psoriasis, 2 weeks of 81 mg low-dose aspirin, a COX-1 inhibitor, reduced serum thromboxane (Tx) B
and reduced brachial vein endothelial proinflammatory transcript expression >70% compared with the no-treatment group (
<0.01). Improvement in brachial vein endothelial cell inflammation significantly correlated with change in serum TxB
(
=0.48,
=0.02).
In patients with psoriasis, platelets are activated and induce endothelial cell inflammation. Low-dose aspirin improved endothelial cell health in psoriasis via platelet COX-1 inhibition. These data demonstrate a previously unappreciated role of platelets in psoriasis and endothelial cell inflammation and suggests that aspirin may be effective in improving vascular health in patients with psoriasis. Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT03228017. |
|---|---|
| AbstractList | Patients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular dysfunction in cardiovascular disease and represent therapeutic targets in cardiovascular prevention. The object of this study was to define the platelet phenotype and effector cell properties on vascular health in psoriasis and evaluate whether aspirin modulates the platelet-induced phenotype. Approach and Results: Platelets from psoriasis patients (n=45) exhibited increased platelet activation (relative to age- and gender-matched controls, n=18), which correlated with psoriasis skin severity. Isolated platelets from psoriasis patients demonstrated a 2- to 3-fold (
<0.01) increased adhesion to human aortic endothelial cells and induced proinflammatory transcriptional changes, including upregulation of
(interleukin 8),
, and Cox (cyclooxygenase)-2 Platelet RNA sequencing revealed an interferon signature and elevated expression of
, which correlated with psoriasis disease severity (
=0.83,
=0.01). In a randomized trial of patients with psoriasis, 2 weeks of 81 mg low-dose aspirin, a COX-1 inhibitor, reduced serum thromboxane (Tx) B
and reduced brachial vein endothelial proinflammatory transcript expression >70% compared with the no-treatment group (
<0.01). Improvement in brachial vein endothelial cell inflammation significantly correlated with change in serum TxB
(
=0.48,
=0.02).
In patients with psoriasis, platelets are activated and induce endothelial cell inflammation. Low-dose aspirin improved endothelial cell health in psoriasis via platelet COX-1 inhibition. These data demonstrate a previously unappreciated role of platelets in psoriasis and endothelial cell inflammation and suggests that aspirin may be effective in improving vascular health in patients with psoriasis. Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT03228017. Patients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular dysfunction in cardiovascular disease and represent therapeutic targets in cardiovascular prevention. The object of this study was to define the platelet phenotype and effector cell properties on vascular health in psoriasis and evaluate whether aspirin modulates the platelet-induced phenotype. Approach and Results: Platelets from psoriasis patients (n=45) exhibited increased platelet activation (relative to age- and gender-matched controls, n=18), which correlated with psoriasis skin severity. Isolated platelets from psoriasis patients demonstrated a 2- to 3-fold (P<0.01) increased adhesion to human aortic endothelial cells and induced proinflammatory transcriptional changes, including upregulation of IL 8 (interleukin 8), IL1β, and Cox (cyclooxygenase)-2 Platelet RNA sequencing revealed an interferon signature and elevated expression of COX-1, which correlated with psoriasis disease severity (r=0.83, P=0.01). In a randomized trial of patients with psoriasis, 2 weeks of 81 mg low-dose aspirin, a COX-1 inhibitor, reduced serum thromboxane (Tx) B2 and reduced brachial vein endothelial proinflammatory transcript expression >70% compared with the no-treatment group (P<0.01). Improvement in brachial vein endothelial cell inflammation significantly correlated with change in serum TxB2 (r=0.48, P=0.02).OBJECTIVEPatients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular dysfunction in cardiovascular disease and represent therapeutic targets in cardiovascular prevention. The object of this study was to define the platelet phenotype and effector cell properties on vascular health in psoriasis and evaluate whether aspirin modulates the platelet-induced phenotype. Approach and Results: Platelets from psoriasis patients (n=45) exhibited increased platelet activation (relative to age- and gender-matched controls, n=18), which correlated with psoriasis skin severity. Isolated platelets from psoriasis patients demonstrated a 2- to 3-fold (P<0.01) increased adhesion to human aortic endothelial cells and induced proinflammatory transcriptional changes, including upregulation of IL 8 (interleukin 8), IL1β, and Cox (cyclooxygenase)-2 Platelet RNA sequencing revealed an interferon signature and elevated expression of COX-1, which correlated with psoriasis disease severity (r=0.83, P=0.01). In a randomized trial of patients with psoriasis, 2 weeks of 81 mg low-dose aspirin, a COX-1 inhibitor, reduced serum thromboxane (Tx) B2 and reduced brachial vein endothelial proinflammatory transcript expression >70% compared with the no-treatment group (P<0.01). Improvement in brachial vein endothelial cell inflammation significantly correlated with change in serum TxB2 (r=0.48, P=0.02).In patients with psoriasis, platelets are activated and induce endothelial cell inflammation. Low-dose aspirin improved endothelial cell health in psoriasis via platelet COX-1 inhibition. These data demonstrate a previously unappreciated role of platelets in psoriasis and endothelial cell inflammation and suggests that aspirin may be effective in improving vascular health in patients with psoriasis. Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT03228017.CONCLUSIONSIn patients with psoriasis, platelets are activated and induce endothelial cell inflammation. Low-dose aspirin improved endothelial cell health in psoriasis via platelet COX-1 inhibition. These data demonstrate a previously unappreciated role of platelets in psoriasis and endothelial cell inflammation and suggests that aspirin may be effective in improving vascular health in patients with psoriasis. Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT03228017. |
| Author | Fisher, Edward A Neimann, Andrea L Lee, Angela Tawil, Michael Eppler, Michael Krueger, James G Garshick, Michael S Mehta, Nehal N Barrett, Tessa J Berger, Jeffrey S Scher, Jose U Jelic, Sanja Salud-Gnilo, Charissa M |
| Author_xml | – sequence: 1 givenname: Michael S surname: Garshick fullname: Garshick, Michael S organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 2 givenname: Michael surname: Tawil fullname: Tawil, Michael organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 3 givenname: Tessa J surname: Barrett fullname: Barrett, Tessa J organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 4 givenname: Charissa M surname: Salud-Gnilo fullname: Salud-Gnilo, Charissa M organization: Laboratory for Investigative Dermatology, Rockefeller University, New York (C.M.S.-G, J.G.K.) – sequence: 5 givenname: Michael surname: Eppler fullname: Eppler, Michael organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 6 givenname: Angela surname: Lee fullname: Lee, Angela organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 7 givenname: Jose U surname: Scher fullname: Scher, Jose U organization: Division of Rheumatology, Department of Medicine, Psoriatic Arthritis Center (J.U.S.), New York University School of Medicine – sequence: 8 givenname: Andrea L surname: Neimann fullname: Neimann, Andrea L organization: Ronald O. Perelman Department of Dermatology (A.L.N.), New York University School of Medicine – sequence: 9 givenname: Sanja surname: Jelic fullname: Jelic, Sanja organization: Division of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, Columbia University Medical Center, New York (S.J.) – sequence: 10 givenname: Nehal N surname: Mehta fullname: Mehta, Nehal N organization: Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD (N.N.M.) – sequence: 11 givenname: Edward A surname: Fisher fullname: Fisher, Edward A organization: Leon H. Charney Division of Cardiology, Department of Medicine (M.S.G., M.T., T.J.B., M.E., A.L., E.A.F., J.S.B.), New York University School of Medicine – sequence: 12 givenname: James G surname: Krueger fullname: Krueger, James G organization: Laboratory for Investigative Dermatology, Rockefeller University, New York (C.M.S.-G, J.G.K.) – sequence: 13 givenname: Jeffrey S surname: Berger fullname: Berger, Jeffrey S organization: Division of Hematology, Department of Medicine (J.S.B.), New York University School of Medicine |
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| Snippet | Patients with psoriasis have impaired vascular health and increased cardiovascular disease (CVD). Platelets are key players in the pathogenesis of vascular... |
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| SubjectTerms | Adult Aspirin - administration & dosage Blood Platelets - drug effects Blood Platelets - enzymology Cells, Cultured Cyclooxygenase 1 - blood Cyclooxygenase 1 - genetics Cyclooxygenase Inhibitors - administration & dosage Endothelial Cells - drug effects Endothelial Cells - enzymology Female Humans Male Middle Aged Platelet Activation Platelet Adhesiveness Psoriasis - blood Psoriasis - diagnosis Psoriasis - drug therapy Psoriasis - enzymology Severity of Illness Index Signal Transduction Thromboxane B2 - blood Treatment Outcome |
| Title | Activated Platelets Induce Endothelial Cell Inflammatory Response in Psoriasis via COX-1 |
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