Genetic Deletion of Polo-Like Kinase 2 Induces a Pro-Fibrotic Pulmonary Phenotype.
Adult
Animals
Cell Proliferation
Cells, Cultured
Collagen
/ metabolism
Female
Fibroblasts
/ enzymology
Gene Deletion
Genetic Predisposition to Disease
Humans
Interleukin-18
/ genetics
Lung
/ enzymology
Male
Mice, 129 Strain
Mice, Knockout
Middle Aged
Myofibroblasts
/ enzymology
Osteopontin
/ genetics
Phenotype
Protein Serine-Threonine Kinases
/ deficiency
Pulmonary Fibrosis
/ enzymology
Signal Transduction
PLK2
fibroblasts
pulmonary fibrosis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
11 03 2021
11 03 2021
Historique:
received:
23
01
2021
revised:
04
03
2021
accepted:
09
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
21
10
2021
Statut:
epublish
Résumé
Pulmonary fibrosis is the chronic-progressive replacement of healthy lung tissue by extracellular matrix, leading to the destruction of the alveolar architecture and ultimately death. Due to limited pathophysiological knowledge, causal therapies are still missing and consequently the prognosis is poor. Thus, there is an urgent clinical need for models to derive effective therapies. Polo-like kinase 2 (PLK2) is an emerging regulator of fibroblast function and fibrosis. We found a significant downregulation of
Identifiants
pubmed: 33799608
pii: cells10030617
doi: 10.3390/cells10030617
pmc: PMC8001503
pii:
doi:
Substances chimiques
IL18 protein, human
0
Interleukin-18
0
SPP1 protein, human
0
Osteopontin
106441-73-0
Collagen
9007-34-5
PLK2 protein, human
EC 2.7.11.-
Protein Serine-Threonine Kinases
EC 2.7.11.1
serum-inducible kinase
EC 2.7.11.21
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany
ID : MeDDrive Start
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