STAT1 regulates macrophage number and phenotype and prevents renal fibrosis after ischemia-reperfusion injury.
Adult
Aged
Animals
Cells, Cultured
Cytokines
/ genetics
Disease Models, Animal
Epithelial Cells
/ metabolism
Female
Fibrosis
Humans
Kidney Diseases
/ genetics
Kidney Tubules
/ metabolism
Macrophage Activation
Macrophages
/ metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
Phenotype
Reperfusion Injury
/ genetics
STAT1 Transcription Factor
/ deficiency
Signal Transduction
STAT1
acute kidney injury
interstitial fibrosis and tubular atrophy
renal fibrosis
renal ischemia-reperfusion injury
Journal
American journal of physiology. Renal physiology
ISSN: 1522-1466
Titre abrégé: Am J Physiol Renal Physiol
Pays: United States
ID NLM: 100901990
Informations de publication
Date de publication:
01 02 2019
01 02 2019
Historique:
pubmed:
8
11
2018
medline:
26
11
2019
entrez:
8
11
2018
Statut:
ppublish
Résumé
Renal ischemia-reperfusion injury (IRI) leads to acute kidney injury or delayed allograft function, which predisposes to fibrosis in the native kidney or kidney transplant. Here we investigated the role of the signal transducer and activator of transcription 1 (STAT1) in inflammatory responses following renal IRI. Our study showed that a subsequent stimulation of Janus-activated kinase 2/STAT1 and Toll-like receptor 4 pathways led to greater STAT1 activation followed by increased cytokine transcription compared with single-pathway stimulation in murine renal tubular cells. Moreover, we observed increased activation of STAT1 under hypoxic conditions. In vivo, STAT1
Identifiants
pubmed: 30403164
doi: 10.1152/ajprenal.00004.2018
doi:
Substances chimiques
Cytokines
0
STAT1 Transcription Factor
0
STAT1 protein, human
0
Stat1 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM