Abstract
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.
Highlights
Spinal cord injury (SCI) is a common affliction of the central ner‐ vous system
Whether LLLT can improve the secretion of neuro‐ trophic factors by macrophages or promote the regrowth of neuronal axons is presently unknown, as well as the mechanism underlying such effects. Starting from these questions, we developed the experiments described in this manuscript to investigate the modulatory effects of LLLT on the secretion of neurotrophic factors by M1 macrophages as well as the underlying molecular mechanisms
Kuo et al 23 used peripheral nerve grafting and admin‐ istration of acidic fibroblast growth factor to the lesion site, which boosted the secretion of brain‐derived neurotrophic fac‐ tor (BDNF) by macrophages within the graft site
Summary
Spinal cord injury (SCI) is a common affliction of the central ner‐ vous system. As result of its high incidence and poor progno‐ sis, SCI has been a major challenge for the medical community.[1]. While the peripheral macrophages, which were differentiated from blood‐derived monocytes massively recruited in the damage area, are the main causes of the further aggravation of the damage in the secondary injury stage.[5] Macrophages are the most important components of the physiological microenvironment at the injury site during the second stage and play an important role in the progression and prognosis of SCI.[6] Recent stud‐ ies have found that different local microenvironments can elicit dif‐ ferent macrophage polarization states and functional phenotypes These phenotypes are typically understood to include the cytotoxic classically activated macrophages (CAMs), termed M1 macrophages, and the anti‐inflammatory, nerve growth‐promoting, alternatively activated macrophages, termed M2 macrophages.[7] Large numbers of macrophages enter the lesion in the immediate period after SCI and are activated to become the M1 type. Starting from these questions, we developed the experiments described in this manuscript to investigate the modulatory effects of LLLT on the secretion of neurotrophic factors by M1 macrophages as well as the underlying molecular mechanisms
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