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• W1994966986 abstract "Glucose is a metabolic regulator of insulin secretion from pancreatic β-cells, which is regulated by intracellular Ca(2+) signaling. We and others previously demonstrated that glucose activates CD38/ADP-ribosyl cyclase (ADPR-cyclase) to produce two Ca(2+) second messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP). Although F-actin remodeling is known to be an important step in glucose stimulated insulin secretion, the role of actin cytoskeleton in regulating Ca(2+) signaling in pancreatic β-cells remain to be solved. Here, we show that actin filaments are involved in the activation of CD38/ADPR-cyclase in pancreatic β-cells. Glucose induces a sequential formation of cADPR and NAADP. Pretreatment with jasplakinolide, an actin polymerizing agent, or a myosin heavy chain IIA (MHCIIA) blocker, blebbistatin, inhibited glucose-induced CD38 internalization, an essential step for cADPR formation. Blocking actin disassembly with jasplakinolide also abrogates glucose-induced cADPR and NAADP formation and sustained Ca(2+) signals. These results indicate that actin filaments along with MHCIIA play an important role in CD38 internalization for the generation of Ca(2+) mobilizing messengers for glucose-induced Ca(2+) signaling in pancreatic β-cells." @default.
• W1994966986 created "2016-06-24" @default.
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• W1994966986 date "2012-03-01" @default.
• W1994966986 modified "2023-09-27" @default.
• W1994966986 title "Involvement of actin filament in the generation of Ca²⁺mobilizing messengers in glucose-induced Ca²⁺signaling in pancreatic β-cells" @default.
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• W1994966986 doi "https://doi.org/10.4161/isl.19490" @default.
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