2021
DOI: 10.1007/s12031-020-01756-9
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Photobiomodulation Promotes Neuronal Axon Regeneration After Oxidative Stress and Induces a Change in Polarization from M1 to M2 in Macrophages via Stimulation of CCL2 in Neurons: Relevance to Spinal Cord Injury

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Cited by 18 publications
(14 citation statements)
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“…These reports agree with our present results, suggesting that ageing enhances the increase in Iba1-IR cell expression in the TG at the onset of ectopic mechanical allodynia in whisker pad skin after IANX. M1 macrophages potentiate inflammation by producing TNF-α, interleukins (IL)-6, and C-C motif chemokine 2 (CCL2) (43)(44)(45). In contrast, M2 macrophages function as antiinflammatory agents by producing anti-inflammatory products such as IL-4, transforming growth factor-β, and CCL4 (46)(47)(48).…”
Section: Discussionmentioning
confidence: 99%
“…These reports agree with our present results, suggesting that ageing enhances the increase in Iba1-IR cell expression in the TG at the onset of ectopic mechanical allodynia in whisker pad skin after IANX. M1 macrophages potentiate inflammation by producing TNF-α, interleukins (IL)-6, and C-C motif chemokine 2 (CCL2) (43)(44)(45). In contrast, M2 macrophages function as antiinflammatory agents by producing anti-inflammatory products such as IL-4, transforming growth factor-β, and CCL4 (46)(47)(48).…”
Section: Discussionmentioning
confidence: 99%
“…Signaling associated with inflammation, such as mitogen-activated protein kinase (MAPK) signaling, nuclear factor kappa-Β (NF-κB) signaling, c-Jun N-terminal kinase (JNK) signaling, and Toll-like receptor (TLR)/myeloid differentiation primary response 88 (MYD88) pathway signaling, is suppressed by PBM; in contrast, the phosphatidylinositol 3-kinase (PI3K)/Akt pathways, extracellular signal-regulated kinase (ERK)/cyclic adenosine monophosphate-responsive element binding protein (CREB) pathways, and transforming growth factor-β (TGF-β)/Smad signaling pathways can be upregulated by PBM [ 59 63 ]. In cultured cells treated with PBM, the expression of GFAP and the secretion of cartilage sulfate proteoglycans (CSPGs) by primary astrocytes are decreased [ 16 ]; the levels of ROS and the axon retraction of dorsal root ganglion (DRG) neurons under oxidative stress conditions are improved [ 64 ]; NF-κB signaling in the activation of M1-type BMDM polarization is inhibited; and the protein kinase A (PKA)/CREB pathway participating in M2 polarization is activated [ 44 , 45 ]. Our findings will contribute to clarification of the biochemical mechanism of PBM, especially since the roles of microglia and astrocytes in neuroinflammation have received increasing attention.…”
Section: Discussionmentioning
confidence: 99%
“…Simultaneously, the exploration of t‐PBM as a novel therapeutic approach for OCD is warranted. This exploration should not be limited to its potential anti‐inflammatory effects in OCD but should also encompass its potential direct impact on neural cells (De Marchi et al., 2021; Esteves et al., 2022; Lima et al., 2014; Lu et al., 2017; Shaikh‐Kader et al., 2021; Zheng et al., 2021). t‐PBM's ability to influence neurons, astrocytes, and microglia through photophysical and photochemical processes in mitochondria‐rich cells offers another avenue of potential therapeutic benefits in OCD (de Freitas & Hamblin, 2016; Dompe et al., 2020; Vieira, Gersten, et al., 2023).…”
Section: Future Directions and Perspectivesmentioning
confidence: 99%