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作 者:Sheng Song Wei Chen Feifan Zhou
机构地区:[1]MOE Key Laboratory of Laser Life Science Institute of Laser Life Science College of Biophotonics,South China Normal University Guangzhou 510631,P.R.China [2]Department of Engineering and Physics University of Central Oklahoma Okilahoma 73034,USA
出 处:《Journal of Innovative Optical Health Sciences》2014年第3期1-10,共10页创新光学健康科学杂志(英文)
基 金:supported by the National Basic Research Program of China(2011CB910402,2010CB732602);the Program for Changjiang Scholars and Innovative Research Team in University(IRT0829);the National Natural Science Foundation of China(30870676,30870658).
摘 要:Microglial activation plays an important role in neurodegenerative diseases.Once activated,they have macrophage-like capabilities,which can be beneficial by phagocytosis and harmful by se-cretion of neurotoxins.However,the resident microglia always fail to trigger an effective pha-gocytic response to clear dead cells or Aβdeposits during the progression of neurodegeneration.Therefore,the regulation of microglial phagocytosis is considered a useful strategy in searchingfor neuroprotective treatments.In this study,our results showed that low-power laser iradiation(LPLI)(20 J/cm²)could enhance microglial phagocytic function in LPS-activated microglia.Wefound that LPLI-mediated microglial phagocytosis is a Rac-1-dependent actin-based process,that a constitutively activated form of Rac1(RaclQ61L)induced a higher level of actin pol-ymerization than cells transfected with wild-type Racl,whereas a dominant negative form ofRacl(RaclT17N)markedly suppressed actin polymerization.In addition,the involvement of Racl activation after LPLI treatment was also observed by using a Raichu fluorescence resonance energy transfer(FRET)-based biosensor.We also found that PI3K/Akt pathway was required inthe LPLI-induced Raci activation.Our research may provide a feasible therapeutic approach tocontrol the progression of neurodegenerative diseases.
关 键 词:MICROGLIA PHAGOCYTOSIS LPLI Racl.
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