Expression data from pancreatic islets of prolactin receptor null pregnant mice

Pancreatic islets adapt to the increase in insulin demand during pregnancy by up-regulating beta cell proliferation, insulin synthesis, and lowering the threshold of glucose-stimulated insulin secretion. In vitro studies suggest that pregnancy hormones, such as placental lactogens and prolactin, both act through the prolactin receptor, are required for these adaptation. Furhtermore, we found that transgenic mice with heterogenous prolactin receptor null mutation are glucose intolerant, with a lower beta-cell mass and lower insulin levels. The goal here is to discover novel targets of prolactin receptor signaling in pancreatic beta cells during pregnancy. Islets were isolated from wild type and heterozygous prolactin receptor knockout mice on day 15 of pregnancy. Islets from each mouse were analyzed separately. After isolation, islets were lysed using the RLT lysis buffer (Qiagen, Valencia, USA) and stored at -80C for RNA extraction.