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

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

FIG. 3.
FIG. 3.

Islet architecture and signal transduction pathways. A: Maintained islet architecture in RIPcre+fakfl/fl islets as assessed by H&E staining and insulin/glucagon immunofluorescent costaining on pancreatic sections from 4–8-week-old mice (original magnification ×20); n = 3 per group. Scale bars, 40 μm. B: α-Cell area was quantified by glucagon-immunostained pancreatic sections and α-cell mass showed a similar level between RIPcre+fakfl/fl mice (■) and RIPcre+fak+/+ littermates (□); n = 3 per genotype. C: Protein analysis by Western blot showed that RIPcre+fakfl/fl islets have attenuated phosphorylated IR, IRS1/2, and Akt compared with RIPcre+fak+/+ littermates. GAPDH, glyceraldehyde-3-phosphate dehydrogenase. D: Protein analysis by Western blot showed that RIPcre+fakfl/fl islets have attenuated ERK1/2 (ERK1 was referred to p44, as presented in the upper band of the Western blot image, and ERK2 was referred to p42, as presented in the bottom band of the image), cyclin D1, CDK5, Bcl-2, Bcl-xL, as well as PDX1, but increased expression of cell cycle inhibitors p53 and p27, compared with RIPcre+fak+/+ littermates. Islets were isolated from 4–8-week-old mice and used for Western blot analysis. Quantification analyses in right panel (□, RIPcre+fak+/+; ■, RIPcre+fakfl/fl); n = 3 per genotype. *P < 0.05; **P < 0.01; ***P < 0.001. Results represent mean ± SE. +,+/+, RIPcre+fak+/+; +,−/−, RIPcre+fakfl/fl. wks, weeks. (A high-quality digital representation of this figure is available in the online issue.)

This Article

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