We examined roles of neurotensin in the dendrite formation and the maturation of dendritic spines in the rat cerebral cortex. Embryonic day (E) 18 cortical neurons were cultured for 2 or 4 days in the presence of neurotensin. The chronic treatment of cortical neurons with neurotensin for 4 days increased the dendritic length of non-GABAergic neurons. In addition, the acute treatment of cortical neurons for 24h at 3 days in vitro also increased the dendritic length of non-GABAergic neurons similarly but more strongly than the chronic treatment. In contrast, the acute treatment for 4h had no effects on the dendrite formation. Next, we examined the effects of neurotensin on the maturation of dendritic spines. E16 cortical neurons were cultured for 10 or 14 days in a basal medium and then treated with neurotensin for 24h. At 11 days in vitro, neurotensin increased the postsynaptic density (PSD) 95-positive dendritic protrusions (filopodia, puncta and spines) together with the increase of spine density and the decrease of puncta density. At 15 days in vitro, neurotensin decreased the puncta density. In addition, the immunohistochemical localization of neurotensin type 1 and type 3 receptors in cultured neurons suggested the differential contribution of the receptors in these effects. These findings suggest that neurotensin promotes the dendrite outgrowth and the maturation of dendritic spines of cultured cortical neurons, although further studies are needed to conclude that these roles of neurotensin are also the case in vivo.
Embryologically, intrahepatic small bile ducts arise from hepatic progenitor cells via ductal plates, whereas the pancreato-extrahepatic biliary progenitor cells expressing the transcription factors PDX1 and HES1 are reportedly involved in the development of the extrahepatic biliary tract and ventral pancreas. The expression of cellular markers characteristic of the different anatomical levels of the biliary tree and pancreas, as well as PDX1 and HES1, was examined in cholangiocarcinoma components of combined hepatocellular cholangiocarcinoma (12 cases), intrahepatic cholangiocarcinoma (21 cases), hilar cholangiocarcinoma (25 cases), and pancreatic ductal adenocarcinoma (18 cases). Anterior gradient protein-2 and S100P were frequently expressed in hilar cholangiocarcinoma and pancreatic ductal adenocarcinoma, whereas neural cell adhesion molecule and luminal expression of epithelial membrane antigen were common in cholangiocarcinoma components of combined hepatocellular cholangiocarcinoma. PDX1 and HES1 were frequently and markedly expressed in pancreatic ductal adenocarcinoma and, to a lesser degree, in hilar cholangiocarcinoma, although their expression was rare and mild in cholangiocarcinoma components in combined hepatocellular cholangiocarcinoma. The expression patterns of these molecules in intrahepatic cholangiocarcinoma were intermediate between those in hilar cholangiocarcinoma and cholangiocarcinoma components of combined hepatocellular cholangiocarcinoma. Pancreatic ductal adenocarcinoma and hilar cholangiocarcinoma had a similar expression of mucin, immunophenotypes, as well as transcription factors. Pancreatic ductal adenocarcinoma and hilar cholangiocarcinoma showed similar postoperative prognosis. In conclusion, the similar expression of phenotypes related to pancreatobiliary anatomy and embryology may in part explain why these 2 types of carcinoma present similar clinicopathologic features. Further studies on the carcinogenesis of these carcinomas based on their similarities are warranted.
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