Involvement of regulatory volume decrease in the migration of nasopharyngeal carcinoma cells

Mao, Jian Wen; Wang, Liwei; Jacob, T. J. C.; Sun, Xue Rong; Li, Hui; Zhu, Lin; Li, Pan; Zhong, Ping; Nie, Si; Chen, Lixin

doi:10.1038/sj.cr.7290304

Cited by 39 publications

(34 citation statements)

References 22 publications

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“…Restitution of isotonicity via RVD is important for maintenance of cell viability and function, e.g., proliferation and migration (Mao et al, 2005;Nilius et al, 1997;Nilius and Wohlrab, 1992;Shen et al, 2003;Shen et al, 2001;Shen et al, 2004). We show here that RVD is accompanied by transient increases in activity of p44/42 and p38MAPK.…”

Section: Discussionmentioning

confidence: 62%

“…Proliferation is also dependent on EGF-induced increases in K + and Cl − conductance, which results in net osmolyte efflux and shrinkage. Previous studies have shown that RVD inhibition-through blockage of K + , Cl − channels and KCC-is capable of hampering cell proliferation and migration (Mao et al, 2005;Nilius et al, 1997;Nilius and Wohlrab, 1992;Shen et al, 2003;Shen et al, 2001;Shen et al, 2004). Therefore, cell proliferation is dependent on coordinated regulation of ion transport pathway activity.…”

Section: Discussionmentioning

confidence: 99%

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Functional and molecular characterization of multiple K–Cl cotransporter isoforms in corneal epithelial cells

Capó-Aponte

Wang

Bildin

et al. 2007

Experimental Eye Research

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The dependence of regulatory volume decrease (RVD) activity on potassium-chloride cotransporter (KCC) isoform expression was characterized in corneal epithelial cells (CEC). During exposure to a 50% hypotonic challenge, the RVD response was larger in SV40-immortalized human CEC (HCEC) than in SV40-immortalized rabbit CEC (RCEC). A KCC inhibitor-[(dihydroindenyl)oxy] alkanoic acid (DIOA)-blocked RVD more in HCEC than RCEC. Under isotonic conditions, Nethylmaleimide (NEM) produced KCC activation and transient cell shrinkage. Both of these changes were greater in HCEC than in RCEC. Immunoblot analysis of HCEC, RCEC, primary human CEC (pHCEC), and primary bovine CEC (BCEC) plasma membrane enriched fractions revealed KCC1, KCC3, and KCC4 isoform expression, whereas KCC2 was undetectable. During a hypotonic challenge, KCC1 membrane content increased more rapidly in HCEC than in RCEC. Such a challenge induced a larger increase and more transient p44/42MAPK activation in HCEC than RCEC. On the other hand, HCEC and RCEC p38MAPK phosphorylation reached peak activations at 2.5 and 15 min, respectively. Only in HCEC, pharmacological manipulation of KCC activity modified the hypotonicity-induced activation of p44/42MAPK, whereas p38MAPK phosphorylation was insensitive to such procedures in both cell lines. Larger increases in HCEC KCC1 membrane protein content correlate with their ability to undergo faster and more complete RVD. Furthermore, pharmacological activation of KCC increased p44/42MAPK phosphorylation in HCEC but not in RCEC, presumably a reflection of low KCC membrane expression in RCEC. These findings suggest that KCC1 plays a role in (i) maintaining isotonic steady-state cell volume homeostasis, (ii) recovery of isotonic cell volume after a hypotonic challenge through RVD, and (iii) regulating hypotonicityinduced activation of the p44/42MAPK signaling pathway required for cell proliferation.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Functional and molecular characterization of multiple K–Cl cotransporter isoforms in corneal epithelial cells

Capó-Aponte

Wang

Bildin

et al. 2007

Experimental Eye Research

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“…In migration assays, chloride conductance is essential for migration in glioma cells, human monocytes, transformed renal epithelial cells, carcinoma cells (CNE-2Z), and microglial cells [7,8,[29][30][31]. Despite these convincing reports on the correlation between chloride conductance and migration, little is known on the impact of chloride conductance on lamellipodium formation.…”

Section: Discussionmentioning

confidence: 99%

Chloride Influx Provokes Lamellipodium Formation in Microglial Cells

Zierler

Frei

Grissmer

et al. 2008

Cell Physiol Biochem

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Lamellipodium extension and retraction is the driving force for cell migration. Although several studies document that activation of chloride channels are essential in cell migration, little is known about their contribution in lamellipodium formation. To address this question, we characterized chloride channels and transporters by whole cell recording and RT-PCR, respectively, as well as quantified lamellipodium formation in murine primary microglial cells as well as the microglial cell-line, BV-2, using time-lapse microscopy. The repertoire of chloride conducting pathways in BV-2 cells included, swelling-activated chloride channels as well as the KCl cotransporters, KCC1, KCC2, KCC3, and KCC4. Swelling-activated chloride channels were either activated by a hypoosmotic solution or by a high KCl saline, which promotes K⁺ and Cl^- influx instead of efflux by KCCs. Conductance through swelling-activated chloride channels was completely blocked by flufenamic acid (200μM), SITS (1mM) and DIOA (10μM). By exposing primary microglial cells or BV-2 cells to a high KCl saline, we observed a local swelling, which developed into a prominent lamellipodium. Blockade of chloride influx by flufenamic acid (200μM) or DIOA (10μM) as well as incubation of cells in a chloride-free high K⁺ saline suppressed formation of a lamellipodium. We assume that local swellings, established by an increase in chloride influx, are a general principle in formation of lamellipodia in eukaryotic cells.

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“…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). Such responses are dependent on receptor mediated differential mitogen protein kinase (MAPK) activation.…”

Section: Introductionmentioning

confidence: 99%

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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Involvement of regulatory volume decrease in the migration of nasopharyngeal carcinoma cells

Cited by 39 publications

References 22 publications

Functional and molecular characterization of multiple K–Cl cotransporter isoforms in corneal epithelial cells

Functional and molecular characterization of multiple K–Cl cotransporter isoforms in corneal epithelial cells

Chloride Influx Provokes Lamellipodium Formation in Microglial Cells

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

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