Glucocorticoids regulate pentraxin-3 expression in human airway smooth muscle cells.
Airway Remodeling
/ genetics
Asthma
/ physiopathology
Bronchi
/ metabolism
C-Reactive Protein
/ genetics
Cells, Cultured
Dexamethasone
/ metabolism
Gene Expression Regulation
/ physiology
Glucocorticoids
/ metabolism
Humans
JNK Mitogen-Activated Protein Kinases
/ metabolism
Lung
/ metabolism
MAP Kinase Signaling System
/ physiology
Mitogen-Activated Protein Kinase 1
/ metabolism
Myocytes, Smooth Muscle
/ metabolism
Phosphorylation
Primary Cell Culture
RNA, Messenger
/ metabolism
Receptors, Glucocorticoid
/ metabolism
Serum Amyloid P-Component
/ genetics
p38 Mitogen-Activated Protein Kinases
/ metabolism
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2019
2019
Historique:
received:
04
03
2019
accepted:
23
07
2019
entrez:
23
8
2019
pubmed:
23
8
2019
medline:
3
3
2020
Statut:
epublish
Résumé
Pentraxin-3 (PTX3) is a multifunctional protein involved in both innate and adaptive immunity. Glucocorticoid (GC) is the first-line therapy to mitigate airway inflammation in asthma. Previous pieces of evidence showed that GC has divergent effects on PTX3 production in various cell types. The molecular mechanisms controlling PTX3 expression in HASMC are, however, not yet characterized. In this study, we demonstrate that the synthetic GC, dexamethasone (DEX) increases the expression of PTX3 both at the protein and mRNA levels. We also found that such an effect of DEX was dependent on de novo protein synthesis and the GC receptor (GR). While DEX increases PTX3 mRNA stability, it did not affect its promoter activity. Interestingly, HASMC pre-treated with p42/p44 ERK inhibitor, but not with p38 or JNK-MAPK inhibitors, significantly interfered with DEX-induced PTX3 secretion. Taken together, our data suggest that GC regulates PTX3 expression in HASMC through transcriptional and post-transcriptional mechanisms in a GR and ERK-dependent manner.
Identifiants
pubmed: 31437159
doi: 10.1371/journal.pone.0220772
pii: PONE-D-19-06339
pmc: PMC6706008
doi:
Substances chimiques
Glucocorticoids
0
RNA, Messenger
0
Receptors, Glucocorticoid
0
Serum Amyloid P-Component
0
PTX3 protein
148591-49-5
Dexamethasone
7S5I7G3JQL
C-Reactive Protein
9007-41-4
JNK Mitogen-Activated Protein Kinases
EC 2.7.11.24
Mitogen-Activated Protein Kinase 1
EC 2.7.11.24
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0220772Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL111541
Pays : United States
Organisme : CIHR
ID : PJT-149062
Pays : Canada
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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