Cell Volume Induced Hormone Secretion: Studies on Signal Transduction and Specificity

Najvirtova, Miroslava; Greer, Susan E.; Greer, Monte A.; Baqi, L; Benický, Július; Štrbák, Vladimír

doi:10.1159/000070255

Cited by 19 publications

(27 citation statements)

References 38 publications

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“…It has already been shown that signaling pathway involved in the cell swelling-induced insulin secretion does not include extracellular Ca 2+ [2,6,7], stretch activated channels [5] 3 or prostaglandins (for review see [7]). Our present experiments demonstrate the independence of swellinginduced insulin release from the intracellular Ca 2+ and PKC as well as its resistance to noradrenaline inhibition.…”

Section: +mentioning

confidence: 99%

Different Signaling Pathways Involved in Glucose- and Cell Swelling-Induced Insulin Secretion by Rat Pancreatic Islets <i>in Vitro</i>

Bačová¹,

Benický²,

Lukyanetz

et al. 2005

Cell Physiol Biochem

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Background: The objective was to compare signal transduction pathways exploited by glucose and cell swelling in stimulating insulin secretion. Methods: Isolated rat (Wistar) pancreatic islets were stimulated in vitro by 20 mmol/l glucose or 30% hypotonic medium (202 mOsm/kg) in various experimental conditions. Results: Glucose did not stimulate insulin release in calcium free medium. Cell swelling-induced insulin release in calcium free medium, even in the presence of the membrane permeable calcium chelator BAPTA/AM (10 µmol/l). Protein kinase C (PKC) inhibitor bisindolylmaleimide VIII (1 µmol/l) abolished the stimulation of insulin secretion by glucose but did not affect the swelling-induced insulin release. PKC activator phorbol 12-13-dibutyrate (1 µmol/l) stimulated insulin secretion in medium containing Ca²⁺ and did not potentiate insulin secretion stimulated by hypotonic extracellular fluid. Dilution of the medium (10-30%) had an additive effect on the glucose-induced insulin secretion. Noradrenaline (1 µmol/l) abolished glucose-induced insulin secretion but did not inhibit hypotonic stimulation either in presence or absence of Ca²⁺. Conclusion: Glucose- and swelling-induce insulin secretion through separate signal transduction pathways. Hyposmotic stimulation is independent from both the extracellular and intracellular Ca²⁺, does not involve PKC activation, and could not be inhibited by noradrenaline. These data indicate a novel signaling pathway for stimulation of insulin secretion exploited by cell swelling.

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Section: +mentioning

confidence: 99%

Different Signaling Pathways Involved in Glucose- and Cell Swelling-Induced Insulin Secretion by Rat Pancreatic Islets <i>in Vitro</i>

Bačová¹,

Benický²,

Lukyanetz

et al. 2005

Cell Physiol Biochem

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“…Secretion of essentially all so-packaged hormones, including pituitary luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, melanocyte-stimulating hormone, thyroid-stimulating hormone, prolactin (Greer et al 1983(Greer et al , 1985(Greer et al , 1990Wang et al 1989;Sato et al 1990aSato et al , 1991, β-endorphin (Back et al 2000), hypothalamic gonadotropin-releasing hormone (Inukai et al 1992), pancreatic insulin (Blackard et al 1975), and glucagon (Blackard et al 1975), is stimulated by cell swelling. Swelling-induced thyrotropin-releasing hormone (TRH) secretion from pancreatic islets (Benicky et al 1997(Benicky et al , 2000, hypothalamic structures (Kucerova & Strbak 2001;Najvirtova et al, 2003;Bacova et al 2006b) and heart (Bacova et al 2006a) was demonstrated. Nevertheless, cell swelling-induced exocytosis possesses lim-1040 R. Hafko et al ited selectivity; cells specifically engaged in water and salt regulation retain their specific response to osmotic stimuli (Najvirtova et al 2003;Bacova et al 2006a,b).…”

Section: Introductionmentioning

confidence: 99%

“…Swelling-induced thyrotropin-releasing hormone (TRH) secretion from pancreatic islets (Benicky et al 1997(Benicky et al , 2000, hypothalamic structures (Kucerova & Strbak 2001;Najvirtova et al, 2003;Bacova et al 2006b) and heart (Bacova et al 2006a) was demonstrated. Nevertheless, cell swelling-induced exocytosis possesses lim-1040 R. Hafko et al ited selectivity; cells specifically engaged in water and salt regulation retain their specific response to osmotic stimuli (Najvirtova et al 2003;Bacova et al 2006a,b).…”

Section: Introductionmentioning

confidence: 99%

Ethanol and urea affect insulin secretion from islets and insulinoma cells by different mechanisms

et al. 2009

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Secretion of insulin could be stimulated by several ways. Comparison of glucose-and swelling-induced mechanisms in pancreatic islets revealed the involvement of a novel signal transduction pathway with specific features of osmotically stimulated peptide hormone release including Ca 2+ independence and resistance to noradrenalin (NA) inhibition. Cell swelling can be induced by hypotonicity or small permeant molecules (e.g. ethanol, urea). Our experiments were aimed to compare the effect of these permeants on insulin secretion from natural system -freshly isolated pancreatic islets and rat insulinoma cell lines INS-1 and INS-1E. As expected glucose and both permeants (80 mM ethanol and urea in isosmotic medium) induced insulin release from islets and NA did not inhibit permeant-induced secretion. Although ethanol and urea induced similar swelling of tumor cells, they produced opposite effect on insulin secretion; while exposure to ethanol led to stimulation of insulin secretion, exposure to urea led to suppression in both types of neoplastic cells. Surprisingly, stimulating effect of ethanol was completely suppressed by NA in both tumor cell lines. Ethanol in hyperosmotic medium failed to stimulate and even inhibited insulin release from both tumor cell lines in present study indicating thus involvement of an osmotic component. In conclusion, the opposite effect of ethanol and urea on insulin secretion from insulinoma cells and sensitivity of ethanol stimulation to NA indicate utilization of different cellular signaling pathways in tumor cells as compared to natural β-cells. Participation of permeant effect in the mechanism of ethanol stimulation remains to be clarified.

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“…Extracellular tonicity, and the associated cell volume regulation, control many molecular and cellular functions including gene expression, neuromediator and hormone release, cell proliferation, apoptosis and migration (Van der Kloot and Molgo 1994;Soroceanu et al 1999;Lang et al 2000;Najvirtova et al 2003;Rouzaire-Dubois et al 2004;Jeon et al 2006;Ernest et al 2008;Okada et al 2009). Independently of protein synthesis, the cell volume (V) is dependent on the external osmolarity and is theoretically described by the Boyle-van't Hoff law: …”

Section: Introductionmentioning

confidence: 99%

Relationship between extracellular osmolarity, NaCl concentration and cell volume in rat glioma cells

Rouzaire‐Dubois¹,

Ouanounou²,

Dubois³

2011

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Abstract. The cell volume, which controls numerous cellular functions, is theoretically linearly related with the inverse osmolarity. However, deviations from this law have often been observed. In order to clarify the origin of these deviations we electronically measured the mean cell volume of rat glioma cells under three different experimental conditions, namely: at different osmolarities and constant NaCl concentration; at different NaCl concentrations and constant osmolarity and at different osmolarities caused by changes in NaCl concentration. In each condition, the osmolarity was maintained constant or changed with NaCl or mannitol. We showed that the cell volume was dependent on both the extracellular osmolarity and the NaCl concentration. The relationship between cell volume, osmolarity and NaCl concentration could be described by a new equation that is the product of the Boyle-van't Hoff law and the Michaelis-Menten equation at a power of 4. Together, these results suggest that in hyponatriemia, the cell volume deviates from the Boyle-van't Hoff law because either the activity of aquaporin 1, expressed in glioma cells, is decreased or the reduced NaCl influx decreases the osmotically obliged influx of water.

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Cell Volume Induced Hormone Secretion: Studies on Signal Transduction and Specificity

Cited by 19 publications

References 38 publications

Different Signaling Pathways Involved in Glucose- and Cell Swelling-Induced Insulin Secretion by Rat Pancreatic Islets <i>in Vitro</i>

Different Signaling Pathways Involved in Glucose- and Cell Swelling-Induced Insulin Secretion by Rat Pancreatic Islets <i>in Vitro</i>

Ethanol and urea affect insulin secretion from islets and insulinoma cells by different mechanisms

Relationship between extracellular osmolarity, NaCl concentration and cell volume in rat glioma cells

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