Here, we report that low-power laser irradiation (LPLI) activates ERK/Sp1 pathway to upregulate VEGF expression and promote vascular endothelial cell proliferation. We demonstrate for the first time that LPLI enhances DNA-binding activity and transactivation activity of Sp1 on VEGF promoter. Additionally, ERK translocates from cytoplasm to
nucleus following LPLI. Moreover, activated ERK phosphorylates Sp1 and results in increased EKR-Sp1 interaction.
Selective inhibition of Sp1 or ERK suppresses the effect of LPLI on the promotion of cell cycle progression and proliferation. These findings provide a novel link between LPLI and angiogenesis, supplying potential therapy strategies
for angiogenesis with LPLI.
Mitochondria are dynamic structures that frequently divide and fuse with one another to form interconnecting network.
This network disintegrates into punctiform organelles during apoptosis. However, it remains unclear whether this event
has a significant impact on the rate of cell death or only accompanies apoptosis as an epiphenomenon. In this study, we
investigate the role of dynamin-related protein 1 (Drp1), a large GTPase that mediates outer mitochondrial membrane
fission, in mitochondrial morphology and apoptosis in response to UV irradiation in human lung adenocarcinoma cells
(ASTC-a-1) and HeLa cells. Using time-lapse fluorescent imaging, we find that Drp1 primarily distributes in cytosol
under physiological conditions. After UV treatment, Drp1 translocates from cytosol to mitochondria, indicating the
enhancement of Drp1 mitochondrial accumulation. Down-regulation of Drp1 by shRNA inhibits UV-induced apoptosis.
Our results suggest that Drp1 is involved in the regulation of transition from a reticulo-tubular to a punctiform
mitochondrial phenotype and mitochondrial fission plays an important role in UV-induced apoptosis.