scholarly journals Ca2+-induced Ca2+Release from the Endoplasmic Reticulum Amplifies the Ca2+Signal Mediated by Activation of Voltage-gated L-type Ca2+Channels in Pancreatic β-Cells

2001 ◽  
Vol 276 (13) ◽  
pp. 9971-9977 ◽  
Author(s):  
Raf Lemmens ◽  
Olof Larsson ◽  
Per-Olof Berggren ◽  
Md. Shahidul Islam
Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3565-3574 ◽  
Author(s):  
Thomas K. Graves ◽  
Patricia M. Hinkle

Abstract The role of the Ca2+-induced Ca2+ release channel (ryanodine receptor) in MIN6 pancreatic β-cells was investigated. An endoplasmic reticulum (ER)-targeted “cameleon” was used to report lumenal free Ca2+. Depolarization of MIN6 cells with KCl led to release of Ca2+ from the ER. This ER Ca2+ release was mimicked by treatment with the ryanodine receptor agonists caffeine and 4-chloro-m-cresol, reversed by voltage-gated Ca2+ channel antagonists and blocked by treatment with antagonistic concentrations of ryanodine. The depolarization-induced rise in cytoplasmic Ca2+ was also inhibited by ryanodine, which did not alter voltage-gated Ca2+ channel activation. Both ER and cytoplasmic Ca2+ changes induced by depolarization occurred in a dose-dependent manner. Glucose caused a delayed rise in cytoplasmic Ca2+ but no detectable change in ER Ca2+. Carbamyl choline caused ER Ca2+ release, a response that was not altered by ryanodine. Taken together, these results provide strong evidence that Ca2+-induced Ca2+ release augments cytoplasmic Ca2+ signals in pancreatic β-cells.


FEBS Letters ◽  
2009 ◽  
Vol 583 (13) ◽  
pp. 2225-2230 ◽  
Author(s):  
Masashi Yoshida ◽  
Katsuya Dezaki ◽  
Shiho Yamato ◽  
Atsushi Aoki ◽  
Hitoshi Sugawara ◽  
...  

Contact ◽  
2019 ◽  
Vol 2 ◽  
pp. 251525641986122 ◽  
Author(s):  
Corina T. Madreiter-Sokolowski ◽  
Roland M. Malli ◽  
Wolfgang F. Graier

This article comments recent publications that highlight an intriguing importance of specific settings in the interaction between the mitochondria and the endoplasmic reticulum to ensure cell-specific functions like the responsiveness to elevated glucose in pancreatic β-cells. Hence, alterations of the mitochondria–endoplasmic reticulum communications under various pathological conditions like aging or cancer often come with enhanced Ca2+ transfer that, in turn, yields stimulation of basal mitochondrial activity to meet the increasing adenosine triphosphate demand of the very cell. Such observations identify mitochondria-associated membranes as potential target for new therapeutic strategies against aging or cancer.


Diabetes ◽  
2009 ◽  
Vol 58 (12) ◽  
pp. 2851-2862 ◽  
Author(s):  
Daniel A. Cunha ◽  
Laurence Ladrière ◽  
Fernanda Ortis ◽  
Mariana Igoillo-Esteve ◽  
Esteban N. Gurzov ◽  
...  

2016 ◽  
Vol 420 (1-2) ◽  
pp. 95-106 ◽  
Author(s):  
Hao-Hao Zhang ◽  
Xiao-Jun Ma ◽  
Li-Na Wu ◽  
Yan-Yan Zhao ◽  
Peng-Yu Zhang ◽  
...  

2005 ◽  
Vol 567 (1) ◽  
pp. 159-175 ◽  
Author(s):  
James Herrington ◽  
Manuel Sanchez ◽  
Denize Wunderler ◽  
Lizhen Yan ◽  
Randal M. Bugianesi ◽  
...  

2018 ◽  
Vol 33 (1) ◽  
pp. 105 ◽  
Author(s):  
Seok-Woo Hong ◽  
Jinmi Lee ◽  
Jung Hwan Cho ◽  
Hyemi Kwon ◽  
Se Eun Park ◽  
...  

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