The aim of the present study was to investigate in vivo whether bone morphogenetic protein-7 (BMP-7) was able to promote and accelerate dental implant healing at a low dose in an osteopenic environment by using a delayed drug-release system. Skeletally mature Chinese goats, having physiologically osteopenic (osteoporotic-like) facial bones, served as an animal model. Dental implants were provided with a delayed-release drug-delivery system and BMP-7 was applied at three different dosages.
View Article and Find Full Text PDFAm J Physiol Gastrointest Liver Physiol
September 2006
Primary cilia are distinct organelles expressed by many vertebrate cells, including cholangiocytes; however, their functions remain obscure. To begin to explore the physiological role of these organelles in the liver, we described the morphology and structure of cholangiocyte cilia and developed new approaches for their isolation. Primary cilia were present only in bile ducts and were not observed in hepatocytes or in hepatic arterial or portal venous endothelial cells.
View Article and Find Full Text PDFIn the PCK rat, a rodent model of Autosomal Recessive Polycystic Kidney Disease (ARPKD), a spontaneous splicing mutation of Pkhd1 initiates hepatic cyst development. Cystic cholangiocytes possess short and malformed cilia that do not express fibrocystin, the Pkhd1 protein. During the disease course, cysts continue to grow; however, the mechanisms underlying cyst progression are unclear due in part to the lack of suitable cell lines to study cystogenesis.
View Article and Find Full Text PDFWith an in vitro model using enclosed intrahepatic bile duct units (IBDUs) isolated from wild-type and somatostatin receptor (SSTR) subtype 2 knockout mice, we tested the effects of somatostatin, secretin, and a selective SSTR2 agonist (L-779976) on fluid movement across the bile duct epithelial cell layer. By RT-PCR, four of five known subtypes of SSTRs (SSTR1, SSTR2A/2B, SSTR3, and SSTR4, but not SSTR5) were detected in cholangiocytes in wild-type mice. In contrast, SSTR2A/2B were completely depleted in the SSTR2 knockout mice whereas SSTR1, SSTR3 and SSTR4 were expressed in these cholangiocytes.
View Article and Find Full Text PDF