Abstract
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, ΔΨm/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.
Highlights
Cell proliferation is a very important physiological effect for low power laser irradiation (LPLI) used in clinical practice
Increased proliferation after LPLI has been shown in many cell types in vitro, including fibroblasts from different systems [1,2,3,4,5,6,7,8], keratinocytes [9], human osteoblasts [10], calvaria osteoblast-like cells [11], lymphocytes [12], mesenchymal stem cells (MSCs) and cardiac stem cells (CSCs) [13], rat Schwann cells [14], aortic smooth muscle cell (SMC) [15], endothelial cells from veins [16] and arteries [17,18], quiescent satellite cells[19,20], human lung adenocarcinoma cells (ASTC-a1) [21] and HeLa cells [22]
We firstly discuss the discovered mitochondrial photoacceptors and nonmitochondrial photoacceptors, respectively; we review the studies on the molecular mechanisms of LPLI-induced proliferation since January 1999, which will serve as a reference for the researchers in this field
Summary
Cell proliferation is a very important physiological effect for low power laser irradiation (LPLI) used in clinical practice. Expression and secretion of molecules induced by LPLI Expression and secretion of growth factors induced by LPLI It has been shown that LPLI significantly increases the gene or protein expressions of several growth factors (Table 1), including brain derived neurotrophic factor (BDNF) and glial derived neurotrophic factor (GDNF) in olfactory ensheathing cells [143], bFGF growth factor production in fibroblasts [144], insulin-like growth factor (IGF)-I in the calvarial cells [145], keratinocyte growth factor (KGF) in human keratinocytes [31], plateletderived growth factor (PDGF) in cultured fibroblasts[146], transforming growth factor- (TGF- ) in the cardiomyocytes [18,147], transforming growth factor- 1 (TGF- 1) [39,148,149], vascular endothelial growth factors (VEGF) by smooth muscle cells, fibroblasts, cardiomyocytes and cardiac myocytes [18,147,150] Among these growth factors, before up-regulation of KGF in keratinocytes [31] and release of TGF- 1 from melanoma cells [39], the researchers examine the immediate increase in m level after light irradiation, which suggests the connection between the elements of mitochondrial retrograde signaling and secondary cellular reactions of expression and secretion of growth factors.
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