Project description:The data present global gene expression profile of whole human bones, implanted in SCID mice (SCID-hu model), then engrafted with the myeloma cell line, Hg, and treated with saline or PTH for 4 weeks. SCID-hu mice were prepared by subcutaneous implantation of human bone in SCID mice. The human myeloma cell line, Hg was injected directly into the implanted bone in SCID-hum mice. Upon establishment of myeloma growth as determined by measurement of circulating human immunoglobulins in SCID-hu mice sera, the mice were treated with saline or intermittent PTH (parathyroid hormone, 80 ug/kg/day) for 4 weeks. At the end of the experiment, the human bones from SCID-hu mice were snap frozen in liquid nitrogen. RNA extracted from these bones was subjected to global gene expression profile using Affymetrix U133-Plus microarray.
Project description:The data present global gene expression profile of whole human bones, implanted in SCID mice (SCID-hu model), then engrafted with the myeloma cell line, Hg, and treated with saline or PTH for 4 weeks.
Project description:Parathyroid hormone (PTH) plays an essential role in regulating calcium and bone homeostasis in the adult, but whether PTH is required at all for regulating fetal-placental mineral homeostasis is uncertain. To address this we treated Pth-null mice in utero with 1 nmol PTH (1-84) or saline and examined placental calcium transfer 90 minutes later. It was found that placental calcium transfer increased in Pth-null fetuses treated with PTH as compared to Pth-null fetuses treated with saline. Subsequently, to determine the effect of PTH treatment on placental gene expression, in a separate experiment, 90 minutes after the fetal injections the placentas were removed for subsequent RNA extraction and microarray analysis.
Project description:Eric Hesse 9 Jan 2019, 17:34 (15 hours ago) to me, Hartmut Lieber Marcel, unten ist das abstract kopiert, reicht das? Lg, Eric Abstract Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.
