Institute of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan, Republic of China.
PLoS One. 2012;7(9):e44027. doi: 10.1371/journal.pone.0044027. Epub 2012 Sep 4.
Low-power laser irradiation (LPLI) has been found to induce various biological effects and cellular processes. Also, LPLI has been shown to promote fracture repair. Until now, it has been unclear how LPLI promotes bone formation and fracture healing. The aim of this study was to investigate the potential mechanism of LPLI-mediated enhancement of bone formation using mouse bone marrow mesenchymal stem cells (D1 cells). D1 cells were irradiated daily with a gallium-aluminum-arsenide (GaAlAs) laser at dose of 0, 1, 2, or 4 J/cm(2). The lactate dehydrogenase (LDH) assay showed no cytotoxic effects of LPLI on D1 cells, and instead, LPLI at 4 J/cm(2) significantly promoted D1 cell proliferation. LPLI also enhanced osteogenic differentiation in a dose-dependent manner and moderately increased expression of osteogenic markers. The neutralization experiments indicated that LPLI regulated insulin-like growth factor 1 (IGF1) and bone morphogenetic protein 2 (BMP2) signaling to promote cell proliferation and/or osteogenic differentiation. In conclusion, our study suggests that LPLI may induce IGF1 expression to promote both the proliferation and osteogenic differentiation of D1 cells, whereas it may induce BMP2 expression primarily to enhance osteogenic differentiation.
低强度激光照射(LPLI)已被发现能诱导各种生物效应和细胞过程。此外,LPLI 已被证明能促进骨折修复。到目前为止,还不清楚 LPLI 如何促进骨形成和骨折愈合。本研究旨在探讨使用小鼠骨髓间充质干细胞(D1 细胞)研究 LPLI 介导增强骨形成的潜在机制。D1 细胞每天用砷化镓铝(GaAlAs)激光照射,剂量为 0、1、2 或 4 J/cm(2)。乳酸脱氢酶(LDH)测定表明,LPLI 对 D1 细胞没有细胞毒性作用,相反,4 J/cm(2)的 LPLI 显著促进了 D1 细胞的增殖。LPLI 还以剂量依赖性方式增强成骨分化,并适度增加成骨标志物的表达。中和实验表明,LPLI 调节胰岛素样生长因子 1(IGF1)和骨形态发生蛋白 2(BMP2)信号通路,促进细胞增殖和/或成骨分化。总之,我们的研究表明,LPLI 可能通过诱导 IGF1 的表达来促进 D1 细胞的增殖和成骨分化,而诱导 BMP2 的表达则主要增强成骨分化。