ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2011
Ca-induced Ca Release from Internal Stores in INS-1 Rat Insulinoma Cells.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Ryanodine Receptors in Islet Cell Function: Calcium Signaling, Hormone Secretion, and Diabetes.Cells · 2025Review
- Research Progress on the Relationship Between Acute Pancreatitis and Calcium Overload in Acinar Cells.Digestive diseases and sciences · 2019Review
- Molecular aspects of intestinal calcium absorption.World journal of gastroenterology · 2015Review
- Article
- Effect of hepcidin on intracellular calcium in human osteoblasts.Molecular and cellular biochemistry · 2012Article
- Alteration of Ryanodine-receptors in Cultured Rat Aortic Smooth Muscle Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Role of regulators of g-protein signaling 4 in ca signaling in mouse pancreatic acinar cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Roles of Non-cholinergic Intrapancreatic Nerves, Serotonergic Nerves, on Pancreatic Exocrine Secretion in the Isolated Perfused Rat Pancreas.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
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Authors and funding
9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The secretion of insulin from pancreatic β-cells is triggered by the influx of Ca(2+) through voltage-dependent Ca(2+) channels. The resulting elevation of intracellular calcium ([Ca(2+)](i)) triggers additional Ca(2+) release from internal stores. Less well understood are the mechanisms involved in Ca(2+) mobilization from internal stores after activation of Ca(2+) influx. The mobilization process is known as calcium-induced calcium release (CICR). In this study, our goal was to investigate the existence of and the role of caffeine-sensitive ryanodine receptors (RyRs) in a rat pancreatic β-cell line, INS-1 cells. To measure cytosolic and stored Ca(2+), respectively, cultured INS-1 cells were loaded with fura-2/AM or furaptra/AM. [Ca(2+)](i) was repetitively increased by caffeine stimulation in normal Ca(2+) buffer. However, peak [Ca(2+)](i) was only observed after the first caffeine stimulation in Ca(2+) free buffer and this increase was markedly blocked by ruthenium red, a RyR blocker. KCl-induced elevations in [Ca(2+)](i) were reduced by pretreatment with ruthenium red, as well as by depletion of internal Ca(2+) stores using cyclopiazonic acid (CPA) or caffeine. Caffeine-induced Ca(2+) mobilization ceased after the internal stores were depleted by carbamylcholine (CCh) or CPA. In permeabilized INS-1 cells, Ca(2+) release from internal stores was activated by caffeine, Ca(2+), or ryanodine. Furthermore, ruthenium red completely blocked the CICR response in permeabilized cells. RyRs were widely distributed throughout the intracellular compartment of INS-1 cells. These results suggest that caffeine-sensitive RyRs exist and modulate the CICR response from internal stores in INS-1 pancreatic β-cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.