T Cell-Derived IL-17A Induces Vascular Dysfunction via Perivascular Fibrosis Formation and Dysregulation of
Animals
Aorta
/ metabolism
Cell Proliferation
Cyclic GMP
/ metabolism
Down-Regulation
Endothelium, Vascular
/ physiopathology
Fibroblasts
/ cytology
Fibrosis
Focal Adhesion Kinase 2
/ metabolism
Interleukin-17
/ genetics
Male
Mice
Mice, Inbred C57BL
Nitric Oxide
/ metabolism
Protein Subunits
/ metabolism
Reactive Oxygen Species
/ metabolism
Signal Transduction
Soluble Guanylyl Cyclase
/ metabolism
T-Lymphocytes
/ cytology
Up-Regulation
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2019
2019
Historique:
received:
10
04
2019
accepted:
27
05
2019
entrez:
10
8
2019
pubmed:
10
8
2019
medline:
4
1
2020
Statut:
epublish
Résumé
The neutrophil recruiting cytokine Interleukin-17A (IL-17A) is a key component in vascular dysfunction and arterial hypertension. Moreover, IL-17A has a central role for the vascular infiltration of myeloid cells into the arterial wall in Angiotensin II-induced vascular inflammation. The intention of our study was to analyze the impact of T cell-derived IL-17A on hypertension, vascular function, and inflammation. Chronic IL-17A overexpression in T cells (CD4-IL-17A Our data demonstrate that T cell-derived IL-17A elicits vascular dysfunction by mediating proliferation of fibroblasts and subsequent vascular fibrosis associated with PYK2 upregulation.
Identifiants
pubmed: 31396305
doi: 10.1155/2019/6721531
pmc: PMC6668561
doi:
Substances chimiques
Interleukin-17
0
Protein Subunits
0
Reactive Oxygen Species
0
Nitric Oxide
31C4KY9ESH
Focal Adhesion Kinase 2
EC 2.7.10.2
Soluble Guanylyl Cyclase
EC 4.6.1.2
Cyclic GMP
H2D2X058MU
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
6721531Déclaration de conflit d'intérêts
The authors declare that they have no conflicts of interest.
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