Activated Platelets Induce Endothelial Cell Inflammatory Response in Psoriasis via COX-1.
Adult
Aspirin
/ administration & dosage
Blood Platelets
/ drug effects
Cells, Cultured
Cyclooxygenase 1
/ blood
Cyclooxygenase Inhibitors
/ administration & dosage
Endothelial Cells
/ drug effects
Female
Humans
Male
Middle Aged
Platelet Activation
Platelet Adhesiveness
Psoriasis
/ blood
Severity of Illness Index
Signal Transduction
Thromboxane B2
/ blood
Treatment Outcome
aspirin
endothelium
inflammation
platelet aggregation
psoriasis
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
pubmed:
7
3
2020
medline:
15
7
2020
entrez:
6
3
2020
Statut:
ppublish
Résumé
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 ( 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.
Identifiants
pubmed: 32131611
doi: 10.1161/ATVBAHA.119.314008
pmc: PMC7180109
mid: NIHMS1565514
doi:
Substances chimiques
Cyclooxygenase Inhibitors
0
Thromboxane B2
54397-85-2
Cyclooxygenase 1
EC 1.14.99.1
PTGS1 protein, human
EC 1.14.99.1
Aspirin
R16CO5Y76E
Banques de données
ClinicalTrials.gov
['NCT03228017']
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1340-1351Subventions
Organisme : NCATS NIH HHS
ID : TL1 TR001447
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001445
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR000053
Pays : United States
Organisme : NHLBI NIH HHS
ID : L30 HL143703
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL098129
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA HL006193
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000040
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL144993
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000038
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR074500
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016087
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL114978
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL139909
Pays : United States
Organisme : NIH HHS
ID : S10 OD019974
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR001446
Pays : United States
Organisme : NHLBI NIH HHS
ID : R56 HL106041
Pays : United States
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