Co‐localization of <i>Nkx6.2</i> and <i>Nkx2.2</i> homeodomain proteins in differentiated myelinating oligodendrocytes

Cai, Jun; Zhu, Qiang; Zheng, Kang; Li, Hong; Qi, Yingchuan; Cao, Qilin; Qiu, Mengsheng

doi:10.1002/glia.20937

Cited by 78 publications

(63 citation statements)

References 31 publications

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“…5 μm frozen sections were immunostained for Nkx2.2 (74.5A5, Developmental Studies Hybridoma Bank, University of Iowa, Iowa city, IA), or for anti-neural glial antigen-2 (NG2, AB5320, Millipore). Nkx2.2 is a homeodomain transcription factor expressed by OPCs that regulates differentiation (Cai et al 2010; Qi et al 2001; Zhu et al 2014). NG2 is a chondroitin sulfate proteoglycan that recognizes OPCs in the intact nervous system (Nishiyama et al 2009).…”

Section: Methodsmentioning

confidence: 99%

Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system

Yoon

Kleven

Paulsen

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Here we show that the interplay between exercise training and dietary fat regulates myelinogenesis in the adult central nervous system. Mice consuming high fat with coordinate voluntary running wheel exercise for 7 weeks showed increases in the abundance of the major myelin membrane proteins, proteolipid (PLP) and myelin basic protein (MBP), in the lumbosacral spinal cord. Expression of MBP and PLP RNA, as well that for Myrf1, a transcription factor driving oligodendrocyte differentiation were also differentially increased under each condition. Furthermore, expression of IGF-1 and its receptor IGF-1R, known to promote myelinogenesis, were also increased in the spinal cord in response to high dietary fat or exercise training. Parallel increases in AKT signaling, a pro-myelination signaling intermediate activated by IGF-1, were also observed in the spinal cord of mice consuming high fat alone or in combination with exercise. Despite the pro-myelinogenic effects of high dietary fat in the context of exercise, high fat consumption in the setting of a sedentary lifestyle reduced OPCs and mature oligodendroglia. Whereas 7 weeks of exercise training alone did not alter OPC or oligodendrocyte numbers, it did reverse reductions seen with high fat. Evidence is presented suggesting that the interplay between exercise and high dietary fat increase SIRT1, PGC-1α and antioxidant enzymes which may permit oligodendroglia to take advantage of diet and exercise-related increases in mitochondrial activity to yield increases in myelination despite higher levels of reactive oxygen species.

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Section: Methodsmentioning

confidence: 99%

Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system

Yoon

Kleven

Paulsen

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Our previous studies demonstrated that Nkx2.2 expression was up-regulated in differentiating OPCs, and disruption of Nkx2.2 gene lead to a dramatic inhibition of oligodendrocyte differentiation and myelin production throughout the CNS [22, 27] . Our recent results with Nkx2.2 conditional mutants suggest that Nkx2.2 is not essential for oligodendrocyte differentiation; instead it controls the timing of differentiation by repressing the expression of PDGFRα directly in OPCs (unpublished observations) possibly by recruiting a repressor complex including HDACs and DNA methyltransferase Dnmt3a [28] .…”

Section: Intracellular Signals That Regulate the Timing Of Oligodendrmentioning

confidence: 99%

Regulation of the timing of oligodendrocyte differentiation: mechanisms and perspectives

et al. 2013

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Axonal myelination is an essential process for normal functioning of vertebrate central nervous system. Proper formation of myelin sheaths around axons depends on the timely differentiation of oligodendrocytes. It was observed that the differentiation occurs on a predictable schedule both in culture and during development. However, the timing mechanisms for oligodendrocyte differentiation during normal development have not been fully uncovered. Recent studies have identified a large number of regulatory factors including the cell-intrinsic factors and extracellular signals that could control the timing of oligodendrocyte differentiation. Here we provide a mechanistic and critical review on the timing control of oligodendrocyte differentiation.

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“…Single or double immunofluorescence on cryostat spinal sections was performed as described previously [28,29]. The images were captured using an epifluorescence microscope (Nikon Eclipse E800).…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Attenuated Reactive Gliosis and Enhanced Functional Recovery Following Spinal Cord Injury in Null Mutant Mice of Platelet-Activating Factor Receptor

et al. 2015

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Platelet-activating factor (PAF) is a unique phosphoglycerine that mediates the biological functions of both immune and nervous systems. Excessive PAF plays an important role in neural injury via its specific receptor (PAFR). In this study, we hypothesized that PAF signaling activates reactive gliosis after spinal cord injury (SCI), and blocking the PAF pathway would modify the glia scar formation and promote functional recovery. PAF microinjected into the normal wild-type spinal cord induced a dose-dependent activation of microglia and astrocytes. In the SCI mice, PAFR null mutant mice showed a better functional recovery in grip and rotarod performances than wild-type mice. Although both microglia and astrocytes were activated after SCI in wild-type and PAFR null mutant mice, expressions of IL-6, vimentin, nestin, and GFAP were not significantly elevated in PAFR null mutants. Disruption of PAF signaling inhibited the expressions of proteoglycan CS56 and neurocan (CSPG3). Intriguingly, compared to the wild-type SCI mice, less axonal retraction/dieback at 7 dpi but more NFH-labeled axons at 28 dpi was found in the area adjacent to the epicenter in PAFR null mutant SCI mice. Moreover, treatment with PAFR antagonist Ginkgolide B (GB) at the chronic phase rather than acute phase enhanced the functional recovery in the wild-type SCI mice. These findings suggest that PAF signaling participates in reactive gliosis after SCI, and blocking of this signaling enhances functional recovery and to some extent may promote axon regrowth.

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Co‐localization of Nkx6.2 and Nkx2.2 homeodomain proteins in differentiated myelinating oligodendrocytes

Cited by 78 publications

References 31 publications

Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system

Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system

Regulation of the timing of oligodendrocyte differentiation: mechanisms and perspectives

Attenuated Reactive Gliosis and Enhanced Functional Recovery Following Spinal Cord Injury in Null Mutant Mice of Platelet-Activating Factor Receptor

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