Process extension and intracellular Ca2+ in cultured murine oligodendrocytes

Yoo, Andrew S.; Krieger, Charles; Kim, Seung Up

doi:10.1016/s0006-8993(99)01282-2

Cited by 28 publications

(34 citation statements)

References 43 publications

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“…Several studies have indicated the importance of Ca 2ϩ in OL process extension (Pende et al, 1997;Stariha et al, 1997;Yoo et al, 1999). Because increased levels of both golli and intracellular Ca 2ϩ levels lead to process outgrowth in OLs, we examined the possibility that the golli effect on process extension was mediated through Ca 2ϩ changes.…”

Section: Process Retraction Results In Local Increases In Intracellulmentioning

confidence: 99%

“…All these data suggest a role for golli on Ca 2ϩ signaling regulation. Several studies have addressed the importance of Ca 2ϩ signaling in OL differentiation and myelination (Soliven, 2001) as well as in process extension and OL migration (Simpson and Armstrong, 1999;Yoo et al, 1999) and retraction of membrane sheets and cell death in mature mouse OLs (Benjamins and Nedelkoska, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Increased Expression of Golli Myelin Basic Proteins Enhances Calcium Influx into Oligodendroglial Cells

Paez¹,

Spreuer²,

Handley³

et al. 2007

J. Neurosci.

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, a specific blocker of voltage-operated Ca 2ϩ channels, abolished the ability of golli to promote process extension in a dose-dependent manner. Analysis of the golli protein identified a myristoylation site at the C terminus of the golli domain, which was essential for the action of golli on Ca 2ϩ influx, suggesting that binding of golli to the plasma membrane is important for modulating Ca 2ϩ homeostasis. High-resolution spatiotemporal analysis along N19 processes revealed higher-amplitude local Ca 2ϩ influx in regions with elevated levels of golli. These findings suggest a key role for golli proteins in regulating voltage-gated Ca 2ϩ channels in OLs during process remodeling. Our observations are consistent with the hypothesis that golli proteins, as a part of a protein complex, modulate Ca 2ϩ influx at the plasma membrane and along OL processes.

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Section: Process Retraction Results In Local Increases In Intracellulmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased Expression of Golli Myelin Basic Proteins Enhances Calcium Influx into Oligodendroglial Cells

Paez¹,

Spreuer²,

Handley³

et al. 2007

J. Neurosci.

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show abstract

“…As with neurons and astrocytes, activation of the IP 3 receptor can cause Ca 2ϩ waves from cell to cell in cultured oligodendrocytes, suggesting that Ca 2ϩ may be important in cell-cell communication (Simpson et al, 1997). Oligodendrocyte process extension in response to PMA (Yoo et al, 1999) and oligodendrocyte migration in response to FGF-2 (Simpson and Armstrong, 1999) are dependent on Ca 2ϩ influx. In studies by Paz , the ability of a monoclonal antibody to promote remyelination in a Theiler's murine encephalomyelitis virus-infected mouse demyelinating model correlated with the ability of these antibodies to induce a Ca 2ϩ influx in isolated oligodendrocytes, suggesting that Ca 2ϩ surges may also be involved in the signal for myelination.…”

Section: Discussionmentioning

confidence: 99%

Region-Specific Myelin Pathology in Mice Lacking the Golli Products of the Myelin Basic Protein Gene

Jacobs

Pribýl²,

Feng³

et al. 2005

J. Neurosci.

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The myelin basic protein (MBP) gene encodes two families of proteins, the classic MBP constituents of myelin and the golli-MBPs, the function of which is less well understood. In this study, targeted ablation of the golli-MBPs, but not the classic MBPs, resulted in a distinct phenotype unlike that of knock-outs (KOs) of the classic MBPs or other myelin proteins. Although the golli KO animals did not display an overt dysmyelinating phenotype, they did exhibit delayed and/or hypomyelination in selected areas of the brain, such as the visual cortex and the optic nerve, as determined by Northern and Western blots and immunohistochemical analysis with myelin protein markers. Hypomyelination in some areas, such as the visual cortex, persisted into adulthood. Ultrastructural analysis of the KOs confirmed both the delay and hypomyelination and revealed abnormalities in myelin structure and in some oligodendrocytes. Abnormal visual-evoked potentials indicated that the hypomyelination in the visual cortex had functional consequences in the golli KO brain. Evidence that the abnormal myelination in these animals was a consequence of intrinsic problems with the oligodendrocyte was indicated by an impaired ability of oligodendrocytes to form myelin sheets in culture and by the presence of abnormal Ca 2ϩ transients in purified cortical oligodendrocytes studied in vitro. The Ca 2ϩ results reported in this study complement previous results implicating golli proteins in modulating intracellular signaling in T-cells. Together, all these findings suggest a role for golli proteins in oligodendrocyte differentiation, migration, and/or myelin elaboration in the brain.

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“…Structure-functionally, CaMKII monomers are composed of four domains, a kinase catalytic, an autoinhibitory (regulatory), an association (oligomerization) domain, and a central variable domain that is subject to alternative splicing and located distal to the autoinhibitory domain (Hudmon and Schulman, 2002). Interestingly, CaMKII␤ has been found to also possess a distinctive actin-binding domain (Okamoto et al, 2009) that has been implicated in mediating actin filament stabilization/bundling (Shen et al, 1998;Fink et al, 2003;O'Leary et al, 2006;Okamoto et al, 2007;Lin and Redmond, 2008). Although primarily characterized in neurons, CaMKII genes, including CaMKII␤, appear to also be expressed by cells of the oligodendrocyte lineage (Cahoy et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

CaMKII Regulates Oligodendrocyte Maturation and CNS Myelination

Waggener

Dupree

Elgersma

et al. 2013

Journal of Neuroscience

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CNS myelination and the maturation of the myelinating cells of the CNS, namely oligodendrocytes, are thought to be regulated by molecular mechanisms controlling the actin cytoskeleton. However, the exact nature of these mechanisms is currently only poorly understood. Here we assessed the role of calcium/calmodulin-dependent kinase type II (CaMKII), in particular CaMKII␤, in oligodendrocyte maturation and CNS myelination. Using in vitro culture studies, our data demonstrate that CaMKII␤ is critical for the proper morphological maturation of differentiating oligodendrocytes, an aspect of oligodendrocyte maturation that is mediated to a large extent by changes in the cellular cytoskeleton. Furthermore, our data provide evidence for an actin-cytoskeleton-stabilizing role of CaMKII␤ in differentiating oligodendrocytes. Using Camk2b knock-out and Camk2b A303R mutant mice, our data revealed an in vivo functional role of CaMKII␤ in regulating myelin thickness that may be mediated by a non-kinase-catalytic activity. Our data point toward a critical role of CaMKII␤ in regulating oligodendrocyte maturation and CNS myelination via an actin-cytoskeleton-regulatory mechanism.

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Process extension and intracellular Ca2+ in cultured murine oligodendrocytes

Cited by 28 publications

References 43 publications

Increased Expression of Golli Myelin Basic Proteins Enhances Calcium Influx into Oligodendroglial Cells

Increased Expression of Golli Myelin Basic Proteins Enhances Calcium Influx into Oligodendroglial Cells

Region-Specific Myelin Pathology in Mice Lacking the Golli Products of the Myelin Basic Protein Gene

CaMKII Regulates Oligodendrocyte Maturation and CNS Myelination

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