Methotrexate Therapy Promotes Cell Coverage and Stability in in-Stent Neointima.
Anaplastic Lymphoma Kinase
/ drug effects
Animals
Apoptosis
/ drug effects
Carotid Artery, Common
/ drug effects
Cell Proliferation
/ drug effects
Disease Models, Animal
Drug-Eluting Stents
/ adverse effects
Endothelial Cells
/ drug effects
Human Umbilical Vein Endothelial Cells
Humans
Inflammation Mediators
/ metabolism
Male
Methotrexate
/ pharmacology
Neointima
/ physiopathology
Phosphatidylinositol 3-Kinases
/ drug effects
Rabbits
Random Allocation
Cell coverage
Inflammation
Neointima
Optical coherence tomography
Stent
Journal
Cardiovascular drugs and therapy
ISSN: 1573-7241
Titre abrégé: Cardiovasc Drugs Ther
Pays: United States
ID NLM: 8712220
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
accepted:
04
12
2020
pubmed:
5
1
2021
medline:
28
1
2022
entrez:
4
1
2021
Statut:
ppublish
Résumé
Anti-proliferative drugs released from drug-eluting stents delay cell coverage and vascular healing, which increases the risk of late stent thrombosis. We assessed the potential effects of systemic methotrexate (MTX) on cell coverage, vascular healing and inflammation activation in vivo and in vitro. We applied MTX in the right common carotid artery in a rabbit stenting model to determine the impact on cell coverage and inflammation activation using a serial optical coherence tomography (OCT) analysis and elucidated the molecular mechanism of MTX in human umbilical vein endothelial cells (HUVECs). Low-dose MTX promoted the development of cell coverage and vascular healing, which was associated with fewer uncovered struts (%) and cross-sections with any uncovered struts (%) at 4 weeks of stenting. The MTX group also exhibited lower rates of heterogeneity, microvessels and per-strut low-signal-intensity layers, indicating neointimal instability at 12 weeks of stenting. In vitro, low-dose MTX strongly inhibited HUVEC apoptosis, promoted proliferation and inhibited inflammatory activation by targeting the phosphoinositide 3-kinase (PI3K)/AKT signalling pathway. Low-dose MTX may be a key means of promoting early cell coverage via the inhibition of the inflammatory response and stability of neointima by targeting inflammatory pathways after stent implantation.
Identifiants
pubmed: 33394362
doi: 10.1007/s10557-020-07121-7
pii: 10.1007/s10557-020-07121-7
doi:
Substances chimiques
Inflammation Mediators
0
Anaplastic Lymphoma Kinase
EC 2.7.10.1
Methotrexate
YL5FZ2Y5U1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
915-925Subventions
Organisme : National Key R&D Program of China
ID : 2016YFC1301100
Organisme : Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang Province, China
ID : KF201811
Organisme : Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang Province, China
ID : KF201916
Organisme : General Undergraduate Colleges and Universities Young Innovative Talents Training Plan, Heilongjiang Province, China
ID : UNPYSCT-2018075
Organisme : Zhejiang Provincial Natural Science Foundation of China
ID : LQ21H020006
Informations de copyright
© 2021. Springer Science+Business Media, LLC, part of Springer Nature.
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