Figure 6

βarr2 inhibited FFAs or glucose-induced activation of the JNK pathway in β-cells. (A) Total RNA was obtained from islets of βarr2^+/+ and βarr2^−/− mice and subjected to whole-genome expression profiling using Affymetrix arrays. Heat diagram depicting genes in the JNK/MAPK pathway for which expression was significantly upregulated (28 genes) and downregulated (7 genes) in the islets of βarr2^−/− as compared with βarr2^+/+ animals (n = 3). (B) Quantification of islet mRNA expression in the JNK pathway normalized with β-actin (n = 4−6). (C) INS-1 (832/13) cells were infected with adenovirus encoding GFP or βarr2 and assayed for p-JNK and total JNK expression in the presence or absence of 30 mmol/L glucose (G30) and 0.4 mmol/L palmate (PA0.4) for 24 h. Pictures are representative of four independent experiments. (D, E) INS-1 (832/13) cells were infected with either adenovirus-encoding shRNA of βarr2 (shβarr2) (D) or βarr2 (E) and incubated with G30 or PA0.4 in the presence of SP600125 (D) or plasmid-expressing JNK (E). Data were presented as fold-change over cells infected with scrambled shRNA (D, white bar) or GFP (E, white bar) (n = 4). *P < 0.05, **P < 0.01, versus indicated group. Muk, mitogen-activated protein kinase upstream protein kinase; Mkk7, mitogen-activated protein kinase kinase 7. Jnk, c-Jun N-terminal kinase.