Cavin-2 Functions as a Suppressive Regulator in TNF-induced Mesenchymal Stromal Cell Inflammation and Angiogenic Phenotypes.
- Author:
Bayader ANNABI
1
;
Alain ZGHEIB
;
Borhane ANNABI
Author Information
- Publication Type:Original Article
- Keywords: Mesenchymal stromal cells; Cavin; TNF; Cancer; Angiogenesis; Inflammation
- MeSH: Gene Silencing; Inflammation*; Mesenchymal Stromal Cells*; Necrosis; Phenotype*; Phosphorylation; Prostaglandin-Endoperoxide Synthases
- From:International Journal of Stem Cells 2017;10(1):103-113
- CountryRepublic of Korea
- Language:English
- Abstract: Tumour necrosis factor (TNF)-α activation of mesenchymal stromal cells (MSC) enhances their tumour-suppressive properties and tumour-homing ability. The molecular actors involved are unknown. We found that TNF induced MSC migration and tubulogenesis which correlated with a dose-dependent increase in Cavin-1 and Cavin-3 transcript levels. TNF triggered cyclooxygenase (COX)-2 expression, whereas specific siRNA-mediated gene silencing of Cavin-2 resulted in an amplified COX-2 expression, tubulogenesis, and migratory response partially due to a rapid and sustained increase in NF-κB phosphorylation status. Our results highlight a suppressive role for the caveolar component Cavin-2 in the angiogenic and inflammatory regulation of TNF-activated MSC.
