Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1
J. Clin. Invest. Jun H. Park, et al. 118:2316 doi:10.1172/JCI33655 [Go to this article.]

Figure 4
USF-1 in IUGR and control islets. (A) ChIP analysis of cross-linked chromatin from islets of IUGR and control animals at fetal day 21, 2 weeks, and 6 months of age IP with antibody to USF-1. Input DNA represents PCR products without prior IP. The IgG IP showed negligible PCR product, indicating little or no IP in the absence of primary antibody. The relative amount of USF-1 bound Pdx1 promoter was measured by Q-PCR and normalized to input DNA. Data are represented as percent of control values. n = 3 experiments, data are ± SEM; *P < 0.05 versus controls. (B) Western blot and densitometric analyses of islets isolated from IUGR and control rats at fetal day 21, 2 weeks, and 6 months of age. Blots were probed with anti–USF-1 and stripped and probed with anti-actin as a control. Data are ± SEM.