2012
DOI: 10.1016/j.nbd.2012.05.001
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Microglial inhibitory factor (MIF/TKP) mitigates secondary damage following spinal cord injury

Abstract: Spinal cord injury (SCI) induces an immune response during which microglia, the resident immunocompetent cells of the central nervous system, become activated and migrate to the site of damage. Depending on their state of activation, microglia secrete neurotoxic or neurotrophic factors that influence the surrounding environment and have a detrimental or restorative effect following SCI, including causing or protecting bystander damage to nearby undamaged tissue. Subsequent infiltration of macrophages contribut… Show more

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Cited by 36 publications
(43 citation statements)
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“…Several anti‐inflammatory drugs have been used in animal studies to reduce the activation of pro‐inflammatory microglia and improve disease outcome. Our lab has shown that targeting microglial function during the secondary phase of SCI (ie, days to weeks after injury) improves the injury outcome by attenuating microglial activation and enhancing oligodendrocyte differentiation and remyelination . Despite this success, there still remains no option to treat SCI during the early phase (ie, first 48 hours).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Several anti‐inflammatory drugs have been used in animal studies to reduce the activation of pro‐inflammatory microglia and improve disease outcome. Our lab has shown that targeting microglial function during the secondary phase of SCI (ie, days to weeks after injury) improves the injury outcome by attenuating microglial activation and enhancing oligodendrocyte differentiation and remyelination . Despite this success, there still remains no option to treat SCI during the early phase (ie, first 48 hours).…”
Section: Introductionmentioning
confidence: 99%
“…Our lab has shown that targeting microglial function during the secondary phase of SCI (ie, days to weeks after injury) improves the injury outcome by attenuating microglial activation and enhancing oligodendrocyte differentiation and remyelination. 13,14 Despite this success, there still remains no option to treat SCI during the early phase (ie, first 48 hours). In this work, we assess the anti-inflammatory effects of 2-phenylethynesulfonamide, a small molecule inhibitor also known as Pifithrinμ (PFTμ), and propose its therapeutic use during the early phase of SCI.…”
mentioning
confidence: 99%
“…In terms of addressing potential shape-dependent toxicity, RhB-labeled α-Fe 2 O 3 N-Rhomb are non-inflammatory and non-cytotoxic at therapeutic concentrations, suggesting that α-Fe 2 O 3 N-Rhomb have the potential to be used as drug carriers. Drugs that either reduce M1 activation or induce M2 activation such as minocycline, tuftsin (TKPR), or microglia inhibitory factor (MIF/TKP) 6769 could be conjugated onto nanoparticles in order to alter the phenotype of microglia. For instance, Papa et al showed that nanostructures conjugated onto minocycline are engulfed by microglia and reduce inflammation in a model of spinal cord injury.…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, CREB and C/EBPbeta cascade may contribute to M2 macrophage-specific gene expression [68]. Inflammatory microglia/macrophages promote secondary injury [69], whereas M2-like macrophages may participate to debris clean-up and remodeling [70], and M2-like microglia may promote oligodendrogenesis [71, 72]. Other report demonstrate that LPS did not affect cell survival of oligodendrocyte precursors, but microglial TLR4 activation by LPS caused oligodendrocyte precursor injury in vivo and in vitro [73].…”
Section: Bidirectional Crosstalk Between Peripheral Cells and Whitmentioning
confidence: 99%