NFAT5/TonEBP Limits Pulmonary Vascular Resistance in the Hypoxic Lung by Controlling Mitochondrial Reactive Oxygen Species Generation in Arterial Smooth Muscle Cells.
Animals
Blood Pressure
Electrocardiography
Gene Expression Regulation
Heart Ventricles
/ diagnostic imaging
Hypoxia
/ pathology
Lung
/ pathology
Metabolome
Mice
Mitochondria
/ metabolism
Myocytes, Smooth Muscle
/ metabolism
Oxidative Phosphorylation
Oxygen Consumption
Protein Transport
Pulmonary Artery
/ pathology
Reactive Oxygen Species
/ metabolism
Systole
Transcription Factors
/ deficiency
Vascular Resistance
/ genetics
NFAT5
mitochondrial ROS
pulmonary artery
smooth muscle cells
transcriptome
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
24 11 2021
24 11 2021
Historique:
received:
19
10
2021
revised:
18
11
2021
accepted:
20
11
2021
entrez:
24
12
2021
pubmed:
25
12
2021
medline:
21
1
2022
Statut:
epublish
Résumé
Chronic hypoxia increases the resistance of pulmonary arteries by stimulating their contraction and augmenting their coverage by smooth muscle cells (SMCs). While these responses require adjustment of the vascular SMC transcriptome, regulatory elements are not well defined in this context. Here, we explored the functional role of the transcription factor nuclear factor of activated T-cells 5 (NFAT5/TonEBP) in the hypoxic lung. Regulatory functions of NFAT5 were investigated in cultured artery SMCs and lungs from control (
Identifiants
pubmed: 34943801
pii: cells10123293
doi: 10.3390/cells10123293
pmc: PMC8699676
pii:
doi:
Substances chimiques
Nfat5 protein, mouse
0
Reactive Oxygen Species
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : 394046768-SFB 1366-A1, A6, B5, C4, Z2
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