Zhonghua nei ke za zhi · 2013
[The mechanism of inhibition of the increase in intracellular calcium concentration by the islet amyloid polypeptide in high glucose-stimulated INS-1 cells].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Yan-yan, Zhu Tie-hong, Liu Ru-ming, He Bing-jun, Zhao Xin, Wang Ying-zi, Li Dai-qing, Xu Yan
Аннотация
OBJECTIVE: To explore the potential mechanism of the inhibition of increased intracellular free calcium concentration ([Ca²⁺]i) by short-term exposure to the islet amyloid polypeptide (IAPP) in high glucose-stimulated pancreatic β cells.
METHODS: The pancreatic β cells were loaded with calcium sensitive fluorescent indicator Fluo-4/AM. The fluorescence intensity, which represented [Ca²⁺]i, was measured in time by laser scanning confocal microscope before and after stimulated by glucose, KCl, caffeine and carbachol.
RESULT: The fluorescence intensity F/F₀ in INS-1 cells, increased to about 2 folds after glucose stimulation. After the exposure to the IAPP with different concentration, the fluorescence intensity F/F₀ was decreased slightly in the pretreated cells by 16.7 mmol/L glucose with 0.5 µmol/L IAPP. However, after the pretreatment of IAPP with the concentration of 1.0, 5.0, 10.0 µmol/L, the fluorescence intensity F/F₀ showed a dose-dependent decrease with statistical difference. The fluorescence intensity F/F₀ in the cells increased rapidly in a peak pattern after the stimulation of 30 mmol/L KCl. But with the pretreatment of 10.0 µmol/L IAPP, the fluorescence intensity F/F₀ decreased with statistical difference. With 20 mmol/L caffeine and 100 µmol/L carbachol which stimulated Ca²⁺ release respectively from internal ryanodine receptor (RYR) and inositol triphosphate (IP₃) Ca²⁺ storage, the fluorescence intensity F/F₀ curve presented a peak pattern. After 10 µmol/L IAPP pretreatment, the fluorescence intensity F/F₀ showed no statistical difference from the control group.
CONCLUSIONS: The short-term effect of IAPP on pancreatic β cells has no influence on the caffeine and carbachol stimulated Ca²⁺ release from endoplasmic reticulum RYR and IP₃ Ca²⁺ storage. The inhibition of calcium increase in INS-1 cells by short-term exposure to IAPP may mainly via inhibiting the voltage-gated L-calcium channels with intact release capacity of Ca²⁺ storage.
METHODS: The pancreatic β cells were loaded with calcium sensitive fluorescent indicator Fluo-4/AM. The fluorescence intensity, which represented [Ca²⁺]i, was measured in time by laser scanning confocal microscope before and after stimulated by glucose, KCl, caffeine and carbachol.
RESULT: The fluorescence intensity F/F₀ in INS-1 cells, increased to about 2 folds after glucose stimulation. After the exposure to the IAPP with different concentration, the fluorescence intensity F/F₀ was decreased slightly in the pretreated cells by 16.7 mmol/L glucose with 0.5 µmol/L IAPP. However, after the pretreatment of IAPP with the concentration of 1.0, 5.0, 10.0 µmol/L, the fluorescence intensity F/F₀ showed a dose-dependent decrease with statistical difference. The fluorescence intensity F/F₀ in the cells increased rapidly in a peak pattern after the stimulation of 30 mmol/L KCl. But with the pretreatment of 10.0 µmol/L IAPP, the fluorescence intensity F/F₀ decreased with statistical difference. With 20 mmol/L caffeine and 100 µmol/L carbachol which stimulated Ca²⁺ release respectively from internal ryanodine receptor (RYR) and inositol triphosphate (IP₃) Ca²⁺ storage, the fluorescence intensity F/F₀ curve presented a peak pattern. After 10 µmol/L IAPP pretreatment, the fluorescence intensity F/F₀ showed no statistical difference from the control group.
CONCLUSIONS: The short-term effect of IAPP on pancreatic β cells has no influence on the caffeine and carbachol stimulated Ca²⁺ release from endoplasmic reticulum RYR and IP₃ Ca²⁺ storage. The inhibition of calcium increase in INS-1 cells by short-term exposure to IAPP may mainly via inhibiting the voltage-gated L-calcium channels with intact release capacity of Ca²⁺ storage.