Unit of Endocrinology and Metabolism, University of Louvain Faculty of Medicine, Brussels, Belgium.
FEBS Lett. 2012 Jan 2;586(1):89-95. doi: 10.1016/j.febslet.2011.11.030. Epub 2011 Dec 3.
Latrunculin depolymerizes and jasplakinolide polymerizes β-cell actin microfilaments. Both increase insulin secretion when Ca(2+) enters β-cells during depolarization by glucose, sulfonylureas or potassium. Mouse islets were held hyperpolarized with diazoxide, and stimulated with acetylcholine to test the role of microfilaments in insulin secretion triggered by intracellular Ca(2+) mobilization and store-operated Ca(2+) entry (SOCE). Jasplakinolide slightly attenuated Ca(2+) mobilization and did not affect SOCE, but consistently inhibited the attending insulin secretion. Latrunculin did not affect Ca(2+) changes induced by acetylcholine, but consistently increased insulin secretion, its effect being larger in response to Ca(2+) entry than to Ca(2+) mobilization. Microfilaments have thus a distinct impact on exocytosis of insulin granules depending on the source of triggering Ca(2+).
拉曲库林使 β 细胞肌动蛋白微丝解聚，而棕桐酰氢醌则使其聚合。当葡萄糖、磺酰脲类或钾离子引起 β 细胞去极化使 Ca2+内流时，这两种药物均能增加胰岛素分泌。用 diazoxide 将胰岛保持超极化，并用乙酰胆碱刺激，以测试微丝在细胞内 Ca2+动员和钙库操纵性钙内流（SOCE）触发的胰岛素分泌中的作用。棕桐酰氢醌轻微减弱 Ca2+动员，但不影响 SOCE，但持续抑制伴随的胰岛素分泌。拉曲库林不影响乙酰胆碱诱导的 Ca2+变化，但持续增加胰岛素分泌，其作用对 Ca2+内流的反应大于对 Ca2+动员的反应。因此，微丝对胰岛素颗粒胞吐的影响取决于触发 Ca2+的来源而不同。
