Migrating Oligodendrocyte Progenitor Cells Swell Prior to Soma Dislocation

Happel, Patrick; Möller, Kerstin; Schwering, Nina K.; Dietzel, Irmgard D.

doi:10.1038/srep01806

Cited by 20 publications

(20 citation statements)

References 76 publications

(120 reference statements)

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“…Previously, we suggested that ion channels like K Ca 3.1 are part of the migratory machinery by inducing localized changes of cell volume (reviewed in [27]). This hydrodynamic model of cell migration was confirmed by other groups [42–44]. Here, we report an additional mechanism by which K Ca 3.1 channels can affect cell migration, namely by cooperating with TRPC3 channels.…”

Section: Discussionsupporting

confidence: 87%

Ion channels in control of pancreatic stellate cell migration

Storck¹,

Hild²,

Schimmelpfennig³

et al. 2016

Oncotarget

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Pancreatic stellate cells (PSCs) play a critical role in the progression of pancreatic ductal adenocarcinoma (PDAC). Once activated, PSCs support proliferation and metastasis of carcinoma cells. PSCs even co-metastasise with carcinoma cells. This requires the ability of PSCs to migrate. In recent years, it has been established that almost all “hallmarks of cancer” such as proliferation or migration/invasion also rely on the expression and function of ion channels. So far, there is only very limited information about the function of ion channels in PSCs. Yet, there is growing evidence that ion channels in stromal cells also contribute to tumor progression. Here we investigated the function of KCa3.1 channels in PSCs. KCa3.1 channels are also found in many tumor cells of different origin. We revealed the functional expression of KCa3.1 channels by means of Western blot, immunofluorescence and patch clamp analysis. The impact of KCa3.1 channel activity on PSC function was determined with live-cell imaging and by measuring the intracellular Ca2+ concentration ([Ca2+]i). KCa3.1 channel blockade or knockout prevents the stimulation of PSC migration and chemotaxis by reducing the [Ca2+]i and calpain activity. KCa3.1 channels functionally cooperate with TRPC3 channels that are upregulated in PDAC stroma. Knockdown of TRPC3 channels largely abolishes the impact of KCa3.1 channels on PSC migration. In summary, our results clearly show that ion channels are crucial players in PSC physiology and pathophysiology.

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Section: Discussionsupporting

confidence: 87%

Ion channels in control of pancreatic stellate cell migration

Storck¹,

Hild²,

Schimmelpfennig³

et al. 2016

Oncotarget

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“…Therefore, a hydrodynamic model was postulated according to which ion channels and transporters elicit local changes of cell volume that act in concert with cytoskeletal mechanisms underlying rear end retraction and/or the protrusion of the cell front [80,87,88]. This model was confirmed experimentally by several groups [89][90][91][92][93]. The observation that aquaporins are essential components of the cellular migration apparatus [94] lent further strong support to this model.…”

Section: Ionic Mechanisms Of Cell Migrationmentioning

confidence: 94%

Ion channels and transporters in tumour cell migration and invasion

Schwab

Stock

2014

Phil. Trans. R. Soc. B

117

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Cell migration is a central component of the metastatic cascade requiring a concerted action of ion channels and transporters (migration-associated transportome), cytoskeletal elements and signalling cascades. Ion transport proteins and aquaporins contribute to tumour cell migration and invasion among other things by inducing local volume changes and/or by modulating Ca 2þ and H þ signalling. Targeting cell migration therapeutically bears great clinical potential, because it is a prerequisite for metastasis. Ion transport proteins appear to be attractive candidate target proteins for this purpose because they are easily accessible as membrane proteins and often overexpressed or activated in cancer. Importantly, a number of clinically widely used drugs are available whose anticipated efficacy as anti-tumour drugs, however, has now only begun to be evaluated.

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“…It has been shown that inhibition of AQP-4 expression negatively affects the migration of astroglia (Kong et al 2008; Saadoun et al 2005). During the process of oligodendrocyte progenitor migration, there is an increase of cell volume in an AQP-4-dependent fashion (Happel et al 2013). In normal cerebral activity, it is important to maintain and stabilize the internal osmotic environment (Simard and Nedergaard 2004).…”

Section: Factors That Enhance the Migration Of Gpsmentioning

confidence: 99%

Migratory potential of transplanted glial progenitors as critical factor for successful translation of glia replacement therapy: The gap between mice and men

Srivastava

Bulte

Walczak

et al. 2017

Glia

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Neurological disorders are a major threat to public health. Stem cell-based regenerative medicine is now a promising experimental paradigm for its treatment, as shown in pre-clinical animal studies. Initial attempts have been on the replacement of neuronal cells only, but glial progenitors (GPs) are now becoming strong alternative cellular therapeutic candidates to replace oligodendrocytes and astrocytes as knowledge accumulates about their important emerging role in various disease processes. There are many examples of successful therapeutic outcomes for transplanted GPs in small animal models, but clinical translation has proved to be challenging due to the 1,000-fold larger volume of the human brain compared to mice. Human GPs transplanted into the mouse brain migrate extensively and can induce global cell replacement, but a similar extent of migration in the human brain would only allow for local rather than global cell replacement. We review here the mechanisms that govern cell migration, which could potentially be exploited to enhance the migratory properties of GPs through cell engineering pre-transplantation. We furthermore discuss the (dis)advantages of the various cell delivery routes that are available, with particular emphasis on intra-arterial injection as the most suitable route for achieving global cell distribution in the larger brain. Now that therapeutic success has proven to be feasible in small animal models, future efforts will need to be directed to enhance global cell delivery and migration to make bench-to-bedside translation a reality.

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Migrating Oligodendrocyte Progenitor Cells Swell Prior to Soma Dislocation

Cited by 20 publications

References 76 publications

Ion channels in control of pancreatic stellate cell migration

Ion channels in control of pancreatic stellate cell migration

Ion channels and transporters in tumour cell migration and invasion

Migratory potential of transplanted glial progenitors as critical factor for successful translation of glia replacement therapy: The gap between mice and men

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