In Vivo Role of Focal Adhesion Kinase in Regulating Pancreatic β-Cell Mass and Function Through Insulin Signaling, Actin Dynamics, and Granule Trafficking

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FIG. 6.
FIG. 6.

Deletion of FAK in β-cells results in impaired actin depolymerization and reduced phosphorylated paxillin (pPaxillin) and talin expression levels. A: F-actin, detected by staining with Alexa Fluor 488–conjugated phalloidin, was depolymerized by high glucose (16.7 mmol/L) in β-cells from RIPcre+fak+/+ (□) but not RIPcre+fakfl/fl (■) mice. Cells were confirmed as β-cells by positive immunostaining for insulin (not shown). The peak intensity of F-actin staining at the plasma membrane was quantified and expressed as arbitrary units (a.u.); n = 72–115 β-cells from three mice for each genotype. HG, high glucose; LG, low glucose. B: Reduced talin expression in RIPcre+fakfl/fl (■) islets compared with RIPcre+fak+/+ (□) littermates; n = 3 per genotype. C: Suppressed phosphorylation of paxillin expression with or without glucose stimulation (15 mmol/L) in RIPcre+fakfl/fl (■) islets compared with RIPcre+fak+/+ (□) littermates as assessed by Western blot. Quantification analyses in bottom panel; n = 3 per genotype. D: β-Cells were stimulated by glucose (15 mmol/L) for 20 min and stained for phospho-paxillin (green) and syntaxin 1 or SNAP-25 (red); n = 3 per genotype (□, RIPcre+fak+/+; ■, RIPcre+fakfl/fl). Scale bars, 5 μm. All mice used in experiments were between 4 and 8 weeks of age. *P < 0.05; **P < 0.01; ***P < 0.001. Results represent mean ± SE. +,+/+, RIPcre+fak+/+; +,−/−, RIPcre+fakfl/fl. (A high-quality digital representation of this figure is available in the online issue.)

This Article

  1. Diabetes vol. 61 no. 7 1708-1718