Molecular mechanisms of cell proliferation induced by low power laser irradiation

被引:385
作者
Gao, Xuejuan
Xing, Da [1 ]
机构
[1] S China Normal Univ, MOE Key Lab Laser Life Sci, Guangzhou 510631, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
PROTEIN-KINASE-C; NITRIC-OXIDE SYNTHASE; NF-KAPPA-B; MAMMALIAN SPERM MITOCHONDRIA; SIGNAL-TRANSDUCTION PATHWAYS; ENDOTHELIAL GROWTH-FACTOR; LIGHT-EMITTING DIODE; SRC TYROSINE KINASE; IN-VITRO; GENE-EXPRESSION;
D O I
10.1186/1423-0127-16-4
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Low power laser irradiation (LPLI) promotes proliferation of multiple cells, which (especially red and near infrared light) is mainly through the activation of mitochondrial respiratory chain and the initiation of cellular signaling. Recently, the signaling proteins involved in LPLI-induced proliferation merit special attention, some of which are regulated by mitochondrial signaling. Hepatocyte growth factor receptor (c-Met), a member of tyrosine protein kinase receptors (TPKR), is phosphorylated during LPLI-induced proliferation, but tumor necrosis factor alpha (TNF-alpha) receptor has not been affected. Activated TPKR could activate its downstream signaling elements, like Ras/Raf/MEK/ERK, PI3K/Akt/eIF4E, PI3K/Akt/eNOS and PLC-gamma/PKC pathways. Other two pathways Delta Psi m/ATP/cAMP/JNK/AP-1 and ROS/Src, are also involved in LPLI-induced proliferation. LPLI-induced cell cycle progression can be regulated by the activation or elevated expressions of cell cycle-specific proteins. Furthermore, LPLI induces the synthesis or release of many molecules, like growth factors, interleukins, inflammatory cytokines and others, which are related to promotive effects of LPLI.
引用
收藏
页数:16
相关论文
共 175 条
[1]
Life-or-death decisions by the Bcl-2 protein family [J].
Adams, JM ;
Cory, S .
TRENDS IN BIOCHEMICAL SCIENCES, 2001, 26 (01) :61-66
[2]
Induction of iNOS expression in skeletal muscle by IL-1β and NFκB activation:: an in vitro and in vivo study [J].
Adams, V ;
Nehrhoff, B ;
Späte, U ;
Linke, A ;
Schulze, PC ;
Baur, A ;
Gielen, S ;
Hambrecht, R ;
Schuler, G .
CARDIOVASCULAR RESEARCH, 2002, 54 (01) :95-104
[3]
Low-level laser therapy decreases levels of lung neutrophils anti-apoptotic factors by a NF-κB dependent mechanism [J].
Aimbire, F. ;
Santos, F. V. ;
Albertini, R. ;
Castro-Faria-Neto, H. C. ;
Mittmann, J. ;
Pacheco-Soares, C. .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2008, 8 (04) :603-605
[4]
Low-level laser therapy induces dose-dependent reduction of TNFα levels in acute inflammation [J].
Aimbire, F ;
Albertini, R ;
Pacheco, MTT ;
Castro-Faria-Neto, HC ;
Leonardo, PSLM ;
Iversen, VV ;
Lopes-Martins, RAB ;
Bjordal, JM .
PHOTOMEDICINE AND LASER SURGERY, 2006, 24 (01) :33-37
[5]
Human fibroblast alterations induced by low power laser irradiation at the single cell level using confocal microscopy [J].
Alexandratou, E ;
Yova, D ;
Handris, P ;
Kletsas, D ;
Loukas, S .
PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 2002, 1 (08) :547-552
[6]
Activation of latent TGF-β1 by low-power laser in vitro correlates with increased TGF-β1 levels in laser-enhanced oral wound healing [J].
Arany, Praveen R. ;
Nayak, Ramakant S. ;
Hallikerimath, Seema ;
Limaye, Anil M. ;
Kale, Alka D. ;
Kondaiah, Paturu .
WOUND REPAIR AND REGENERATION, 2007, 15 (06) :866-874
[7]
CYCLIN D1 IS A NUCLEAR-PROTEIN REQUIRED FOR CELL-CYCLE PROGRESSION IN G(1) [J].
BALDIN, V ;
LUKAS, J ;
MARCOTE, MJ ;
PAGANO, M ;
DRAETTA, G .
GENES & DEVELOPMENT, 1993, 7 (05) :812-821
[8]
LOW-INTENSITY LASER THERAPY - STILL NOT AN ESTABLISHED CLINICAL TOOL [J].
BASFORD, JR .
LASERS IN SURGERY AND MEDICINE, 1995, 16 (04) :331-342
[9]
NEW BIOLOGICAL PHENOMENA ASSOCIATED WITH LASER-RADIATION [J].
BELKIN, M ;
SCHWARTZ, M .
HEALTH PHYSICS, 1989, 56 (05) :687-690
[10]
Low-energy laser irradiation affects satellite cell proliferation and differentiation in vitro (vol 1448, pg 372, 1999) [J].
Ben-Dov, N ;
Shefer, G ;
Irintchev, A ;
Wernig, A ;
Oron, U ;
Halevy, O .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 1999, 1450 (01) :108-108