Masha Roland T, Houreld Nicolette N, Abrahamse Heidi
Laser Research Centre, Faculty of Health Sciences, University of Johannesburg , Doornfontein, Johannesburg, South Africa.
Photomed Laser Surg. 2013 Feb;31(2):47-53. doi: 10.1089/pho.2012.3369. Epub 2012 Dec 16.
Low-intensity laser irradiation (LILI) has been shown to stimulate cellular functions leading to increased adenosine triphosphate (ATP) synthesis. This study was undertaken to evaluate the effect of LILI on genes involved in the mitochondrial electron transport chain (ETC, complexes I-IV) and oxidative phosphorylation (ATP synthase).
Four human skin fibroblast cell models were used in this study: normal non-irradiated cells were used as controls while wounded, diabetic wounded, and ischemic cells were irradiated. Cells were irradiated with a 660 nm diode laser with a fluence of 5 J/cm(2) and gene expression determined by quantitative real-time reverse transcription (RT) polymerase chain reaction (PCR).
LILI upregulated cytochrome c oxidase subunit VIb polypeptide 2 (COX6B2), cytochrome c oxidase subunit VIc (COX6C), and pyrophosphatase (inorganic) 1 (PPA1) in diabetic wounded cells; COX6C, ATP synthase, H+transporting, mitochondrial Fo complex, subunit B1 (ATP5F1), nicotinamide adenine dinucleotide (NADH) dehydrogenase (ubiquinone) 1 alpha subcomplex, 11 (NDUFA11), and NADH dehydrogenase (ubiquinone) Fe-S protein 7 (NDUFS7) in wounded cells; and ATPase, H+/K+ exchanging, beta polypeptide (ATP4B), and ATP synthase, H+ transporting, mitochondrial Fo complex, subunit C2 (subunit 9) (ATP5G2) in ischemic cells.
LILI at 660 nm stimulates the upregulation of genes coding for subunits of enzymes involved in complexes I and IV and ATP synthase.
低强度激光照射（LILI）已被证明可刺激细胞功能，导致三磷酸腺苷（ATP）合成增加。本研究旨在评估LILI对参与线粒体电子传递链（ETC，复合体I-IV）和氧化磷酸化（ATP合酶）的基因的影响。
本研究使用了四种人类皮肤成纤维细胞模型：正常未照射细胞用作对照，而受伤、糖尿病伤口和缺血细胞进行照射。用波长660nm、能量密度5J/cm²的二极管激光照射细胞，并通过定量实时逆转录（RT）聚合酶链反应（PCR）测定基因表达。
LILI上调了糖尿病伤口细胞中的细胞色素c氧化酶亚基VIb多肽2（COX6B2）、细胞色素c氧化酶亚基VIc（COX6C）和焦磷酸酶（无机）1（PPA1）；上调了受伤细胞中的COX6C、ATP合酶、H⁺转运、线粒体F₀复合体、亚基B1（ATP5F1）、烟酰胺腺嘌呤二核苷酸（NADH）脱氢酶（泛醌）1α亚复合体、11（NDUFA11）和NADH脱氢酶（泛醌）铁硫蛋白7（NDUFS7）；上调了缺血细胞中的ATP酶、H⁺/K⁺交换、β多肽（ATP4B）和ATP合酶、H⁺转运、线粒体F₀复合体、亚基C2（亚基9）（ATP5G2）。
660nm的LILI刺激了参与复合体I和IV以及ATP合酶的酶亚基编码基因的上调。
