| First Author | Henquin JC | Year | 2012 |
| Journal | FEBS Lett | Volume | 586 |
| Issue | 1 | Pages | 89-95 |
| PubMed ID | 22154597 | Mgi Jnum | J:180514 |
| Mgi Id | MGI:5306520 | Doi | 10.1016/j.febslet.2011.11.030 |
| Citation | Henquin JC, et al. (2012) Disruption and stabilization of beta-cell actin microfilaments differently influence insulin secretion triggered by intracellular Ca2+ mobilization or store-operated Ca2+ entry. FEBS Lett 586(1):89-95 |
| abstractText | Latrunculin depolymerizes and jasplakinolide polymerizes beta-cell actin microfilaments. Both increase insulin secretion when Ca(2+) enters beta-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+). |
