A silver lining of neuroinflammation: Beneficial effects on myelination

Goldstein, Evan Z.; Church, Jamie S.; Hesp, Zoe C.; Popovich, Phillip G.; McTigue, Dana M.

doi:10.1016/j.expneurol.2016.05.001

Cited by 36 publications

(30 citation statements)

References 163 publications

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“…The release of Ccl2 and Ccl3, as well as signalling through Ccr2 and Ccr5 can promote the migration, proliferation, differentiation, and survival of neural progenitor cells35. A transient and controlled level of neuroinflammation can also promote myelin debris clearance, myelin repair36, angiogenesis37, and amyloid beta (Aβ) plaque clearance38. When inflammation becomes chronic, however, the production of Tnfα, Il6, and reactive oxygen species within the CNS act to suppress neurogenesis and leads to apoptosis and neurodegenerative processes35.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of focused ultrasound-induced increases in blood-brain barrier permeability on rat microvascular transcriptome

McMahon

Bendayan

Hynynen

2017

Sci Rep

109

110

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Therapeutic treatment options for central nervous system diseases are greatly limited by the blood-brain barrier (BBB). Focused ultrasound (FUS), in conjunction with circulating microbubbles, can be used to induce a targeted and transient increase in BBB permeability, providing a unique approach for the delivery of drugs from the systemic circulation into the brain. While preclinical research has demonstrated the utility of FUS, there remains a large gap in our knowledge regarding the impact of sonication on BBB gene expression. This work is focused on investigating the transcriptional changes in dorsal hippocampal rat microvessels in the acute stages following sonication. Microarray analysis of microvessels was performed at 6 and 24 hrs post-FUS. Expression changes in individual genes and bioinformatic analysis suggests that FUS may induce a transient inflammatory response in microvessels. Increased transcription of proinflammatory cytokine genes appears to be short-lived, largely returning to baseline by 24 hrs. This observation may help to explain some previously observed bioeffects of FUS and may also be a driving force for the angiogenic processes and reduced drug efflux suggested by this work. While further studies are necessary, these results open up intriguing possibilities for novel FUS applications and suggest possible routes for pharmacologically modifying the technique.

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Section: Discussionmentioning

confidence: 99%

Acute effects of focused ultrasound-induced increases in blood-brain barrier permeability on rat microvascular transcriptome

McMahon

Bendayan

Hynynen

2017

Sci Rep

109

110

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“…Myelin and oligodendrocytes are susceptible to injury or disease which causes myelin damage [12]. This damage leads to axonal dysfunction, pathology and pronounced neurologic impairment.…”

Section: Introductionmentioning

confidence: 99%

“…The promotion of remyelination by oligodendrocyte progenitor cells (OPCs) and/or oligodendrocytes has been difficult to achieve, and remains a major obstacle in MS [13]. The influence of neuroinflammation on oligodendrocytes and OPCs is complex, with both detrimental and beneficial properties [12]. Oligodendrocytes are particularly sensitive to the effects of IFN-γ, which can inhibit remyelination through modulation of ER stress [14,15].…”

Section: Introductionmentioning

confidence: 99%

Role of the JAK/STAT signaling pathway in regulation of innate immunity in neuroinflammatory diseases

Yan

Gibson

Buckley

et al. 2018

Clinical Immunology

209

125

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The Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) signaling pathway is utilized by numerous cytokines and interferons, and is essential for the development and function of both innate and adaptive immunity. Aberrant activation of the JAK/STAT pathway is evident in neuroinflammatory diseases such as Multiple Sclerosis and Parkinson’s Disease. Innate immunity is the front line defender of the immune system and is composed of various cell types, including microglia, macrophages and neutrophils. Innate immune responses have both pathogenic and protective roles in neuroinflammation, depending on disease context and the microenvironment in the central nervous system. In this review, we discuss the role of innate immunity in the pathogenesis of neuroinflammatory diseases, how the JAK/STAT signaling pathway regulates the innate immune response, and finally, the potential for ameliorating neuroinflammation by utilization of JAK/STAT inhibitors.

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“…Peripheral nerves are playing an irreplaceable role in connecting the central nervous system with the sensory and motor organs, while their injury is still a very common clinical trauma that may lead to significant loss of sensory and motor functions (Li X. et al, 2010; Goldstein et al, 2016). Peripheral nerve injury (PNI) can induce complex pathophysiological processes and inflammatory response which are important in regulating the repair process of exacerbating tissue damage or promoting tissue repair (Siqueira Mietto et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Epidermal Neural Crest Stem Cells on Local Inflammation Microenvironment in the Defected Sciatic Nerve of Rats

Dongdong

Liu

et al. 2017

Front. Mol. Neurosci.

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Cell-based therapy is a promising strategy for the repair of peripheral nerve injuries (PNIs). epidermal neural crest stems cells (EPI-NCSCs) are thought to be important donor cells for repairing PNI in different animal models. Following PNI, inflammatory response is important to regulate the repair process. However, the effects of EPI-NCSCs on regulation of local inflammation microenviroment have not been investigated extensively. In the present study, these effects were studied by using 10 mm defected sciatic nerve, which was bridged with 15 mm artificial nerve composed of EPI-NCSCs, extracellular matrix (ECM) and poly (lactide-co-glycolide) (PLGA). Then the expression of pro- and anti-inflammatory cytokines, polarization of macrophages, regulation of fibroblasts and shwann cells (SCs) were assessed by western blot, immunohistochemistry, immunofluorescence staining at 1, 3, 7 and 21 days after bridging. The structure and the function of the bridged nerve were determined by observation under light microscope and by examination of right lateral foot retraction time (LFRT), sciatic function index (SFI), gastrocnemius wet weight and electrophysiology at 9 weeks. After bridging with EPI-NCSCs, the expression of anti-inflammatory cytokines (IL-4 and IL-13) was increased, but decreased for pro-inflammatory cytokines (IL-6 and TNF-α) compared to the control bridging, which was consistent with increase of M2 macrophages and decrease of M1 macrophages at 7 days after transplantation. Likewise, myelin-formed SCs were significantly increased, but decreased for the activated fibroblasts in their number at 21 days. The recovery of structure and function of nerve bridged with EPI-NCSCs was significantly superior to that of DMEM. These results indicated that EPI-NCSCs could be able to regulate and provide more suitable inflammation microenvironment for the repair of defected sciatic nerve.

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A silver lining of neuroinflammation: Beneficial effects on myelination

Cited by 36 publications

References 163 publications

Acute effects of focused ultrasound-induced increases in blood-brain barrier permeability on rat microvascular transcriptome

Acute effects of focused ultrasound-induced increases in blood-brain barrier permeability on rat microvascular transcriptome

Role of the JAK/STAT signaling pathway in regulation of innate immunity in neuroinflammatory diseases

The Effects of Epidermal Neural Crest Stem Cells on Local Inflammation Microenvironment in the Defected Sciatic Nerve of Rats

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