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Low‐level laser therapy 810‐nm up‐regulates macrophage secretion of neurotrophic factors via PKA‐CREB and promotes neuronal axon regeneration in vitro
Author(s) -
Zhang Jiawei,
Sun Jiakai,
Zheng Qiao,
Hu Xueyu,
Wang Zhe,
Liang Zhuowen,
Li Kun,
Song Jiwei,
Ding Tan,
Shen Xuefeng,
Zhang Jianxin,
Qiao Lin
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14756
Subject(s) - neurotrophic factors , secretion , axon , regeneration (biology) , creb , macrophage , neurotrophin , low level laser therapy , microbiology and biotechnology , lesion , macrophage polarization , cancer research , medicine , neuroscience , chemistry , in vitro , biology , pathology , transcription factor , receptor , laser , biochemistry , laser therapy , physics , gene , optics
Macrophages play key roles in the secondary injury stage of spinal cord injury (SCI). M1 macrophages occupy the lesion area and secrete high levels of inflammatory factors that hinder lesion repair, and M2 macrophages can secrete neurotrophic factors and promote axonal regeneration. The regulation of macrophage secretion after SCI is critical for injury repair. Low‐level laser therapy (810‐nm) (LLLT) can boost functional rehabilitation in rats after SCI; however, the mechanisms remain unclear. To explore this issue, we established an in vitro model of low‐level laser irradiation of M1 macrophages, and the effects of LLLT on M1 macrophage polarization and neurotrophic factor secretion and the related mechanisms were investigated. The results showed that LLLT irradiation decreased the expression of M1 macrophage‐specific markers, and increased the expression of M2 macrophage‐specific markers. Through forward and reverse experiments, we verified that LLLT can promote the secretion of various neurotrophic factors by activating the PKA‐CREB pathway in macrophages and finally promote the regeneration of axons. Accordingly, LLLT may be an effective therapeutic approach for SCI with clinical application prospects.

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