Relative contribution of chloride channels and transporters to regulatory volume decrease in human glioma cells

Ernest, Nola Jean; Weaver, Amy K.; Duyn, Lauren B. Van; Sontheimer, Harald

doi:10.1152/ajpcell.00503.2004

Cited by 106 publications

(112 citation statements)

References 47 publications

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“…The contribution of this alternative mechanism to RVD is variable in different species, but less than that mediated by Cl − and K + channel activity. These individual contributions by different ion transport mechanisms to RVD are similar to what has been reported in human glioma cells (Ernest et al, 2005).…”

Section: Discussionsupporting

confidence: 86%

“…On the other hand, the fact that the suppressions of RVD were greater in Cl − -free and high-K + solutions (53 and 44%, respectively) than those obtained with individual Cl − and K + channel inhibitors (27% and 27%, respectively), suggests the existence of a heterogeneous family of volume-sensitive ion transients mechanisms, only some of which are sensitive to NA and 4-AP (Nilius et al, 1996). KCl cotransporter (KCC) is another type of contributor to RVD, which has been described in multiple cell lines, including HCEC and RCEC (Capo-Aponte et al, 2005, 2007aErnest et al, 2005;Lauf and Adragna, 2000;Shen et al, 2000;Wehner et al, 2003). The contribution of this alternative mechanism to RVD is variable in different species, but less than that mediated by Cl − and K + channel activity.…”

Section: Discussionmentioning

confidence: 99%

“…In some epithelia, this efflux results from activation of volume-sensitive K + , Cl − channels (Grunnet et al, 2002;Hazama and Okada, 1988;Pavenstadt et al, 1996;Shen et al, 2001). Another contributor to RVD in human CEC (HCEC) and some other tissues is the K-Cl cotransporter (KCC) (Capo-Aponte et al, 2005, 2007aErnest et al, 2005). Even though volume sensitive Cl − channel activity was identified in many tissues, nothing is known about the role of K + as a counterion to Cl − egress in RCEC (AlNakkash et al, 2004;Dupre-Aucouturier et al, 2004;Hazama and Okada, 1988;Inoue et al, 2005) The ability of cells to regulate their cellular volume during exposure to an anisosmotic challenge is essential for sustaining their proliferative (Lang et al, 2005;Schreiber, 2005), migratory (Mao et al, 2005;Soroceanu et al, 1999) and secretory activity (Do et al, 2006;Strbak and Greer, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

Pan¹,

Capó-Aponte²,

Zhang³

et al. 2007

Experimental Eye Research

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We characterized the dependence of hypotonicity-induced regulatory volume decrease (RVD) responses on mitogen-activated protein kinase (MAPK) pathway signaling in SV40-immortalized rabbit corneal epithelial cells (RCEC). Following calcein-AM loading, RVD was monitored using a microplate fluorescence reader. Western blot analysis determined MAPK activation. After 30 min, the RVD response restored the relative cell volume to nearly isotonic values, whereas it was inhibited when cells were bathed either in a Cl − -free solution or with the Cl − -channel inhibitors: 5-nitro-2-(3-phenylpropylamino) benzoic acid or niflumic acid. Similar declines occurred with either a high-K + (20 mM) supplemented solution or the K + channel inhibitor 4-aminopyridine. Activation of extracellular signal-regulated kinase (ERK), p38, and stress-activated protein kinase/c-Jun Nterminal kinase (SAPK/JNK) was time and tonicity-dependent. Stimulation of ERK and SAPK/JNK was maximized earlier than that of p38. Activation of ERK and SAPK/JNK was insensitive to Cl − and K + channel inhibitors, whereas inhibition with either PD98059 or SP600125, respectively, blocked RVD. However, inhibition of p38 with SB203580 had no effect on RVD. Suppression of RVD instead blocked p38 activation. Differences in the dependence of RVD activation on Erk1/2 and p38 signaling were validated in dominant negative (d/n) -Erk1 and d/n-p38 cells. Volumesensitive Cl − and K + channel activation contributes, in concert, to RVD in RCEC. Therefore, swelling-induced ERK and SAPK/JNK stimulation precedes Cl − and K + channel activation, whereas p38 activation occurs as a consequence of RVD.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

Pan¹,

Capó-Aponte²,

Zhang³

et al. 2007

Experimental Eye Research

View full text Add to dashboard Cite

show abstract

“…Of course, this begs the question of how Cl − is pumped into these cells. It is believed that Cl − uptake generally occurs via the NKCC transporter (Russell, 2000), which is the primary transporter in glioma cells (Ernest and Sontheimer, 2005), and is balanced by Cl − efflux via KCC transporters. In neurons, the shift from accumulation of Cl − in immature, migratory cells to a passive Cl − distribution in differentiated, post-migratory cells occurs by the developmental insertion of KCC2 transporters .…”

Section: Discussionmentioning

confidence: 99%

“…In neurons, the shift from accumulation of Cl − in immature, migratory cells to a passive Cl − distribution in differentiated, post-migratory cells occurs by the developmental insertion of KCC2 transporters . In glioma cells, the Cl − equilibrium is maintained by NKCC and KCC1 and KCC3a transporters (Ernest et al, 2005;Ernest and Sontheimer, 2005). Accordingly, cell migration should be disrupted if the Cl − gradient of these cells is disrupted, and that is indeed observed in glioma cells when the permeant Cl − ion is replaced with impermeant anions (Soroceanu et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

A role for ion channels in glioma cell invasion

McFerrin¹,

2005

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Many cells, including neuronal and glial progenitor cells, stem cells and microglial cells, have the capacity to move through the extracellular spaces of the developing and mature brain. This is particularly pronounced in astrocyte-derived tumors, gliomas, which diffusely infiltrate the normal brain. Although a significant body of literature exists regarding signals that are involved in the guidance of cells and their processes, little attention has been paid to cell-shape and cell-volume changes of migratory cells. However, extracellular spaces in the brain are very narrow and represent a major obstacle that requires cells to dynamically regulate their volume. Recent studies in glioma cells show that this involves the secretion of Cl − and K + with water. Pharmacological inhibition of Cl − channels impairs their ability to migrate and limits tumor progression in experimental tumor models. One Cl − -channel inhibitor, chlorotoxin, is currently in Phase II clinical trials to treat malignant glioma. This article reviews our current knowledge of cell-volume changes and the role of ion channels during the migration of glioma cells. It also discusses evidence that supports the importance of channel-mediated cell-volume changes in the migration of immature neurons and progenitor cells during development. New unpublished data is presented, which demonstrates that Cl − and K + channels involved in cell shrinkage localize to lipid-raft domains on the invadipodia of glioma cells and that their presence might be regulated by trafficking of these proteins in and out of lipid rafts.

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4D Printing for Vascular Tissue Engineering: Progress and Challenges

Zeenat

Zolfagharian

Yeleswarapu

et al. 2023

Adv Materials Technologies

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The hierarchical network of blood vessels comprises the larger vessels (veins and arteries), the smaller ones (venules and arterioles), and the thinnest capillaries. The proper functioning of most tissues in the body relies on vascularization, which is meant for the diffusion of gases, nutrients, and harmful waste. However, it is known that cell survival is compromised as the diffusion of oxygen is limited beyond 100–200 µm and damage can occur at any level of the complex system of the vascular network, as is the case in cardiovascular, musculoskeletal, and neurovascular diseases that recur and progress with age. These may prove fatal, hence the need for vascular tissue engineering (VTE) arises. VTE mainly focuses on the fabrication of vascular constructs using natural, synthetic material, or a combination of both using various techniques. The construct is expected to integrate and anastomose with the host vasculature. 4D bioprinting is an emerging field that allows the fabrication of hollow tubes employing different materials that respond to different stimuli. This review is a comprehensive summary of the major techniques employed in VTE and the recent technique of 4D bioprinting foreseen to revolutionize the field.

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Relative contribution of chloride channels and transporters to regulatory volume decrease in human glioma cells

Abstract: Relative contribution of chloride channels and transporters to regulatory volume decrease in human glioma cells.

Cited by 106 publications

References 47 publications

Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

A role for ion channels in glioma cell invasion

4D Printing for Vascular Tissue Engineering: Progress and Challenges

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