Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells

Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulate...
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Autor*in:	Suarez Castellanos, Ivan [verfasserIn] Singh, Tania Balteanu, Bogdan Bhowmick, Diti Chatterjee Jeremic, Aleksandar Zderic, Vesna

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Anmerkung:	© The Author(s). 2017

Übergeordnetes Werk:	Enthalten in: Journal of Therapeutic Ultrasound - London : Biomed Central, 2013, 5(2017), 1 vom: 05. Dez.
Übergeordnetes Werk:	volume:5 ; year:2017 ; number:1 ; day:05 ; month:12

Links:	Volltext

DOI / URN:	10.1186/s40349-017-0108-9

Katalog-ID:	SPR036361917

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520			\|a Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner.
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allfields	10.1186/s40349-017-0108-9 doi (DE-627)SPR036361917 (SPR)s40349-017-0108-9-e DE-627 ger DE-627 rakwb eng Suarez Castellanos, Ivan verfasserin aut Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. Singh, Tania aut Balteanu, Bogdan aut Bhowmick, Diti Chatterjee aut Jeremic, Aleksandar aut Zderic, Vesna aut Enthalten in Journal of Therapeutic Ultrasound London : Biomed Central, 2013 5(2017), 1 vom: 05. Dez. (DE-627)745616321 (DE-600)2714301-6 2050-5736 nnns volume:5 year:2017 number:1 day:05 month:12 https://dx.doi.org/10.1186/s40349-017-0108-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2017 1 05 12
spelling	10.1186/s40349-017-0108-9 doi (DE-627)SPR036361917 (SPR)s40349-017-0108-9-e DE-627 ger DE-627 rakwb eng Suarez Castellanos, Ivan verfasserin aut Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. Singh, Tania aut Balteanu, Bogdan aut Bhowmick, Diti Chatterjee aut Jeremic, Aleksandar aut Zderic, Vesna aut Enthalten in Journal of Therapeutic Ultrasound London : Biomed Central, 2013 5(2017), 1 vom: 05. Dez. (DE-627)745616321 (DE-600)2714301-6 2050-5736 nnns volume:5 year:2017 number:1 day:05 month:12 https://dx.doi.org/10.1186/s40349-017-0108-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2017 1 05 12
allfields_unstemmed	10.1186/s40349-017-0108-9 doi (DE-627)SPR036361917 (SPR)s40349-017-0108-9-e DE-627 ger DE-627 rakwb eng Suarez Castellanos, Ivan verfasserin aut Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. Singh, Tania aut Balteanu, Bogdan aut Bhowmick, Diti Chatterjee aut Jeremic, Aleksandar aut Zderic, Vesna aut Enthalten in Journal of Therapeutic Ultrasound London : Biomed Central, 2013 5(2017), 1 vom: 05. Dez. (DE-627)745616321 (DE-600)2714301-6 2050-5736 nnns volume:5 year:2017 number:1 day:05 month:12 https://dx.doi.org/10.1186/s40349-017-0108-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2017 1 05 12
allfieldsGer	10.1186/s40349-017-0108-9 doi (DE-627)SPR036361917 (SPR)s40349-017-0108-9-e DE-627 ger DE-627 rakwb eng Suarez Castellanos, Ivan verfasserin aut Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. Singh, Tania aut Balteanu, Bogdan aut Bhowmick, Diti Chatterjee aut Jeremic, Aleksandar aut Zderic, Vesna aut Enthalten in Journal of Therapeutic Ultrasound London : Biomed Central, 2013 5(2017), 1 vom: 05. Dez. (DE-627)745616321 (DE-600)2714301-6 2050-5736 nnns volume:5 year:2017 number:1 day:05 month:12 https://dx.doi.org/10.1186/s40349-017-0108-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2017 1 05 12
allfieldsSound	10.1186/s40349-017-0108-9 doi (DE-627)SPR036361917 (SPR)s40349-017-0108-9-e DE-627 ger DE-627 rakwb eng Suarez Castellanos, Ivan verfasserin aut Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. Singh, Tania aut Balteanu, Bogdan aut Bhowmick, Diti Chatterjee aut Jeremic, Aleksandar aut Zderic, Vesna aut Enthalten in Journal of Therapeutic Ultrasound London : Biomed Central, 2013 5(2017), 1 vom: 05. Dez. (DE-627)745616321 (DE-600)2714301-6 2050-5736 nnns volume:5 year:2017 number:1 day:05 month:12 https://dx.doi.org/10.1186/s40349-017-0108-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2017 1 05 12
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The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Singh, Tania</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Balteanu, Bogdan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bhowmick, Diti Chatterjee</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jeremic, Aleksandar</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zderic, Vesna</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of Therapeutic Ultrasound</subfield><subfield code="d">London : Biomed Central, 2013</subfield><subfield code="g">5(2017), 1 vom: 05. 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author	Suarez Castellanos, Ivan
spellingShingle	Suarez Castellanos, Ivan Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
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topic_title	Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
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title	Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
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title_full	Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
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author_browse	Suarez Castellanos, Ivan Singh, Tania Balteanu, Bogdan Bhowmick, Diti Chatterjee Jeremic, Aleksandar Zderic, Vesna
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title_sort	calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
title_auth	Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
abstract	Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. © The Author(s). 2017
abstractGer	Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. © The Author(s). 2017
abstract_unstemmed	Background Our previous studies have indicated that ultrasound can stimulate the release of insulin from pancreatic beta cells, providing a potential novel treatment for type 2 diabetes. The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner. © The Author(s). 2017
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title_short	Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells
url	https://dx.doi.org/10.1186/s40349-017-0108-9
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author2	Singh, Tania Balteanu, Bogdan Bhowmick, Diti Chatterjee Jeremic, Aleksandar Zderic, Vesna
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The purpose of this study was to explore the temporal dynamics and $ Ca^{2+} $-dependency of ultrasound-stimulated secretory events from dopamine-loaded pancreatic beta cells in an in vitro setup. Methods Carbon fiber amperometry was used to detect secretion from INS-1832/13 beta cells in real time. The levels of released insulin were also measured in response to ultrasound treatment using insulin-specific ELISA kit. Beta cells were exposed to continuous wave 800 kHz ultrasound at intensities of 0.1 W/$ cm^{2} $, 0.5 W/$ cm^{2} $ and 1 W/$ cm^{2} $ for several seconds. Cell viability tests were done with trypan blue dye exclusion test and MTT analysis. Results Carbon fiber amperometry experiments showed that application of 800 kHz ultrasound at intensities of 0.5 and 1 W/$ cm^{2} $ was capable of stimulating secretory events for durations lasting as long as the duration of the stimulus. Furthermore, the amplitude of the detected peaks was reduced by 64% (p < 0.01) when extracellular $ Ca^{2+} $ was chelated with 10 mM EGTA in cells exposed to ultrasound intensity of 0.5 W/$ cm^{2} $. Measurements of released insulin in response to ultrasound stimulation showed complete inhibition of insulin secretion by chelating extracellular $ Ca^{2+} $ with 10 mM EGTA (p < 0.01). Viability studies showed that 800 kHz, 0.5 W/$ cm^{2} $ ultrasound did not cause any significant effects on viability and metabolic activity in cells exposed to ultrasound as compared to sham-treated cells. Conclusions Our results demonstrated that application of ultrasound was capable of stimulating the release of insulin from pancreatic beta cells in a safe, controlled and $ Ca^{2+} $-dependent manner.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Singh, Tania</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Balteanu, Bogdan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bhowmick, Diti Chatterjee</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jeremic, Aleksandar</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zderic, Vesna</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of Therapeutic Ultrasound</subfield><subfield code="d">London : Biomed Central, 2013</subfield><subfield code="g">5(2017), 1 vom: 05. 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Calcium-dependent ultrasound stimulation of secretory events from pancreatic beta cells

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