Figure 2.

ROS-mediated activation of RTKs signaling cascades by UV irradiation. (Upper panel) In absence of UV irradiation (basal conditions), RTKs and downstream signaling in skin cells are maintained in a low state of activation by protein tyrosine phosphatase activities that dynamically dephosphorylate RTKs. These conditions favor normal collagen synthesis and low production of matrix metalloproteinases (MMPs). (Lower panel) Absorption of UV irradiation energy by skin cell components, in the presence of molecular oxygen, generates reactive oxygen species (ROS) that react with cysteine in the catalytic site of protein tyrosine phosphatases. Inhibition of protein tyrosine phosphatases by reaction with ROS increases net RTK phosphorylation levels and triggers downstream signaling cascades that include mitogen-activated protein kinase (MAPK) phosphorylation and activation of activator protein-1 (AP-1) transcription factor. Activated AP-1 represses collagen production and increases MMP gene transcription. As a result, UV irradiation induces transient collagen deficit.