A distinct mechanism of senescence activation in amnion epithelial cells by infection, inflammation, and oxidative stress.

Christopher Luke DixonLauren RichardsonSamantha Sheller-MillerGeorge SaadeRamkumar Menon

Published in: American journal of reproductive immunology (New York, N.Y. : 1989) (2017)

TNF-α caused OS-mediated p38MAPK induction, senescence, and IL-6 increase from AECs. LPS also induced senescence and IL-6 increase. Inflammatory and infectious factors may cause premature fetal cell senescence contributing to preterm birth pathophysiology.

Keyphrases

oxidative stress
dna damage
preterm birth
endothelial cells
diabetic rats
stress induced
high glucose
low birth weight
single cell
inflammatory response
induced apoptosis
cell therapy
gestational age
stem cells
preterm infants
mesenchymal stem cells
endoplasmic reticulum stress
drug induced