Role of JNK-1 regulation in the protection of contact-inhibited fibroblasts from oxidative stress.

The molecular signaling events leading to protection from oxidative stress-induced apoptosis upon contact inhibition have not been fully investigated. Previous research has indicated a role for mitogen-activated protein kinases (MAPKs) in the regulation of contact inhibition, and these proteins have also been associated with cell cycle regulation and stress-induced apoptosis. The potential role of the MAPK JNK-1 in the stress-response of actively proliferating and contact-inhibited cells was investigated.

Attenuation of p38 MAPK activity upon contact inhibition in fibroblasts.

The molecular events, which govern growth control upon contact inhibition have not yet been clearly defined. Previous work has indicated that there is an increase in the expression of mitogen-activated protein kinase phosphatases (MKPs) upon the attainment of contact inhibition in normal fibroblasts, concurrently with a decrease in ERK activity. To investigate the potential role of p38 and JNK in the transition to a contact-inhibited state, normal human fibroblasts (BJ) were grown to subconfluent and confluent densities.