PMID- 23804320 OWN - NLM STAT- MEDLINE DCOM- 20131209 LR - 20171116 IS - 1097-4652 (Electronic) IS - 0021-9541 (Linking) VI - 229 IP - 1 DP - 2014 Jan TI - Activated ERK/FOXM1 pathway by low-power laser irradiation inhibits UVB-induced senescence through down-regulating p21 expression. PG - 108-16 LID - 10.1002/jcp.24425 [doi] AB - Cellular senescence is a growth-arrest program that limits cell proliferation. Low-power laser irradiation (LPLI) has been demonstrated to promote cell proliferation. However, whether LPLI can inhibit cellular senescence remains unknown. In the present study, to investigate the functional role of LPLI against skin aging, we used ultraviolet radiation b (UVB) to induce cell senescence. We first report that LPLI can delay UVB-induced cell senescence. The senescence-associated beta-galactosidase (SA-beta-Gal) activity and p21 expression, hallmarks of senescent cells, were decreased in the Forkhead box transcription factor FOXM1-dependent manner under treatment with LPLI. The effect of LPLI was further enhanced with an overexpression of FOXM1, and abolished when FOXM1 was knockdown with short hairpin RNA (shRNA). Furthermore, LPLI activated the extracellular regulated protein kinases (ERK) that was upstream of FOXM1. This led to FOXM1 phosphorylation and nuclear translocation. Nuclear translocation enhanced FOXM1 transcriptional activity and promoted its downstream target gene c-Myc expression that could inhibit p21 expression. These findings highlight the protective effects of ERK/FOXM1 pathway against UVB-induced cell senescence, suggesting a potential protecting strategy for treating skin aging by LPLI. CI - (c) 2013 Wiley Periodicals, Inc. FAU - Ling, Qingzhou AU - Ling Q AD - MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou, China. FAU - Meng, Chengbo AU - Meng C FAU - Chen, Qun AU - Chen Q FAU - Xing, Da AU - Xing D LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Cell Physiol JT - Journal of cellular physiology JID - 0050222 RN - 0 (Forkhead Box Protein M1) RN - 0 (Forkhead Transcription Factors) RN - 0 (Foxm1 protein, mouse) SB - IM MH - Adult MH - Animals MH - Apoptosis/radiation effects MH - Cell Proliferation/radiation effects MH - Cellular Senescence/*radiation effects MH - Fibroblasts/radiation effects MH - Forkhead Box Protein M1 MH - Forkhead Transcription Factors/*metabolism MH - Humans MH - *Low-Level Light Therapy MH - MAP Kinase Signaling System/radiation effects MH - Mice MH - NIH 3T3 Cells MH - Phosphorylation/radiation effects MH - Skin Aging/genetics/*radiation effects MH - *Ultraviolet Rays EDAT- 2013/06/28 06:00 MHDA- 2013/12/16 06:00 CRDT- 2013/06/28 06:00 PHST- 2013/04/15 00:00 [received] PHST- 2013/06/20 00:00 [accepted] PHST- 2013/06/28 06:00 [entrez] PHST- 2013/06/28 06:00 [pubmed] PHST- 2013/12/16 06:00 [medline] AID - 10.1002/jcp.24425 [doi] PST - ppublish SO - J Cell Physiol. 2014 Jan;229(1):108-16. doi: 10.1002/jcp.24425.