Osmosignalling in C6 glioma cells

Sinning, Ralf; Schliess, Freimut; Kubitz, Ralf; Häussinger, Dieter

doi:10.1016/s0014-5793(96)01376-2

Cited by 52 publications

(27 citation statements)

References 45 publications

(61 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Swelling increases IP 3 turnover in rabbit proximal tubule cells [35], in COS-7 cells [39]and in airway epithelium [42], but in other cells such changes do not occur [43]or are only marginal or appear with a time course unrelated to the [Ca 2+ ] i elevation [44]. Further evidence against a causal relationship between IP 3 generation and the [Ca 2+ ] i elevation by swelling comes from reports showing a failure of the phospholipase C blocker U-73122 to prevent the osmosensitive [Ca 2+ ] i increase [45, 46]. Conversely, in Ehrlich ascites cells, an increase in IP 3 formation without [Ca 2+ ] i elevation is elicited by swelling [47].…”

Section: [Ca2+]i Elevation Subsequent To Swelling: Sources and Mechanmentioning

confidence: 99%

“…The specific proteins involved in the tyrosine kinase signalling cascade are still unknown. Activation of the Erk1/Erk2 has been observed in association with hyposmotic swelling in human intestine 407 cell line, C6 glioma cells and cortical astrocytes [45, 46, 106, 107]. However, only in astrocytes, phosphorylation of these kinases has been directly linked with the activation of an osmosensitive Cl – current [107].…”

Section: Calcium and Osmosignallingmentioning

confidence: 99%

See 1 more Smart Citation

Influence of Calcium on Regulatory Volume Decrease: Role of Potassium Channels

Pasantes‐Morales¹,

Mulia²

2000

Nephron

View full text Add to dashboard Cite

In most cell types, hyposmotic swelling consistently elicits an increase in the concentration of cytosolic Ca²⁺ – [Ca²⁺]_i – with contributions of extracellular and intracellular sources. The mechanisms of Ca²⁺ entry and release from endogenous sources are not fully clarified and may be cell specific. The ubiquity of the swelling-evoked [Ca²⁺]_i rise makes Ca²⁺ a likely candidate for a role as osmotransducing signal. However, the regulatory volume decrease (RVD) which follows swelling and the osmolyte fluxes involved in this process are not always Ca²⁺ dependent. It was found that, with a few exceptions, in most cell types the osmosensitive Cl^– efflux pathway and the swelling-activated organic osmolyte fluxes are Ca²⁺ independent. In contrast, Ca²⁺-dependent or Ca²⁺-independent K⁺ fluxes activated by swelling are detected, depending on the cell type. The close correlation found in this review between the Ca²⁺ dependence of RVD and that of the K⁺ channels activated by swelling led to the conclusion that it is the type of osmosensitive K⁺ pathway which largely confers the Ca²⁺ dependence to RVD. Interestingly, this coincidence of Ca²⁺-dependent K⁺ efflux and RVD is found predominantly in epithelial cells, whereas in nonepithelial cells both processes are largely Ca²⁺ independent. In these cells, the [Ca²⁺]_i rise elicited by swelling may be an epiphenomenon.

show abstract

Section: [Ca2+]i Elevation Subsequent To Swelling: Sources and Mechanmentioning

confidence: 99%

Section: Calcium and Osmosignallingmentioning

confidence: 99%

Influence of Calcium on Regulatory Volume Decrease: Role of Potassium Channels

Pasantes‐Morales¹,

Mulia²

2000

Nephron

View full text Add to dashboard Cite

show abstract

“…Hypotonicity-induced activation of Erk-1/2 MAP kinases has been reported for all mammalian cell types studied so far, including Intestine 407 cells [11,32], H4IIE hepatoma cells [33], primary rat hepatocytes [34], cardiac myocytes [35], astrocytes [13,36], C6 glioma cells [37], isolated rat pancreatic acini [38] and mIMCD3 renal cells [39]. In addition, in Intestine 407 cells and many other cell models, hypo-osmotic cell swelling also leads to the activation of p38 and JNK MAP kinases [35,[39][40][41][42].…”

Section: Hypotonicity-provoked Activation Of Map Kinasesmentioning

confidence: 99%

“…In addition, in Intestine 407 cells and many other cell models, hypo-osmotic cell swelling also leads to the activation of p38 and JNK MAP kinases [35,[39][40][41][42]. Unlike the activation of Mpk1p in yeast, the activation of Erk-1/2 by osmotic cell swelling is independent of protein kinase C [32][33][34][36][37][38], but, in Intestine 407 cells, involves p21Ras and Raf1 [32].…”

Section: Hypotonicity-provoked Activation Of Map Kinasesmentioning

confidence: 99%

Signalling Mechanisms Involved in Volume Regulation of Intestinal Epithelial Cells

Wijk

Tomassen

Jonge

et al. 2000

Cell Physiol Biochem

View full text Add to dashboard Cite

Most mammalian cells have developed compensatory mechanisms to respond to the variable osmotic stress caused by changes in the concentrations of intracellular osmo-active substances (e.g. glucose, amino acids, lactate) or by variations in the osmolarity of the surrounding medium. In response to osmotic cell swelling, the Regulatory Volume Decrease (RVD) is triggered and directs a reduction in the tonicity of the cell by the concerted opening of cation and anion selective ion channels. To date, the K⁺ and Cl^- conductances activated upon hypo-osmotic stimulation have been characterised electrophysiologically in many different cell systems. The molecular identity of the channels however, as well as the mechanism(s) involved in their activation have not yet been fully clarified and may differ between cell types. In this review, we will evaluate the different signalling pathways activated by osmotic cell swelling and discuss their putative role(s) in ion channel regulation, in maintaining cellular volume homeostasis, and in auto- and paracrinic signal transduction, with emphasis on intestinal epithelial cells.

show abstract

“…MAPK pathways are activated by tyrosine phosphorylation induced by diverse extracellular stimuli, e.g., anisosmotic challenge, mechanical stress, and growth factors. Hypotonicity-induced swelling is accompanied by a rapid and transient increase of tyrosine phosphorylation of multiple proteins, including p44/42 (i.e., Erk1/2) and p38MAPK (Noe et al, 1996;Sadoshima et al, 1996;Schliess et al, 1995;Schliess et al, 1996;Sinning et al, 1997;Tilly et al, 1996a;Tilly et al, 1996b;Zhang et al, 1998). Moreover, increased tyrosine phosphorylation was found to be a critical step in activating the RVD process (Tilly et al, 1996a;Tilly et al, 1993).…”

Section: Introductionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Osmosignalling in C6 glioma cells

Cited by 52 publications

References 45 publications

Influence of Calcium on Regulatory Volume Decrease: Role of Potassium Channels

Influence of Calcium on Regulatory Volume Decrease: Role of Potassium Channels

Signalling Mechanisms Involved in Volume Regulation of Intestinal Epithelial Cells

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

Contact Info

Product

Resources

About