Project description:The effect of parathyroid hormone (PTH) analog treatment was tested on osteoblasts prepared from calvaria of C57BL/6J mice 7-10 days old. Osteoblasts were treated for 4 hr with either human parathyroid hormone (1-34) (hPTH(1-34), bovine (D-Trp12,Tyr34)-PTH(7-34) amide (bPTH(7-34)), bPTH(3-34), hPTH(1-31), or hPTH(7-34). Gene expression effects were evaluated by DNA microarray.
Project description:The effect of parathyroid hormone (PTH) treatment was tested on osteoblasts prepared from calvaria of C57BL/6J mice 7-10 days old. Osteoblasts were treated with either human parathyroid hormone (1-34), bovine (D-Trp12,Tyr34) parathyroid hormone (7-34) amide or vehicle control for 4 hr. Gene expression effects were evaluated by DNA microarray.
Project description:Pulmonary hypertension (PH) is an incurable right heart failure disease. Parathyroid hormone (PTH) is secreted from the parathyroid gland and plays a crucial role in calcium homeostasis. PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We assessed whether the regulation of PTH affected PH in a hypoxia (Hx)-induced PH mouse model. PTH treatment exacerbated right ventricular hypertrophy and right ventricular systolic pressure in Hx mice. Our data showed how is PTH effected for PH model murine lung.
Project description:The aim of this study was to explore the involvement of long noncoding RNAs (lncRNAs) during intermittent parathyroid hormone (PTH) induced cementogenesis.
Project description:The energetic costs of bone formation require osteoblasts to coordinate their activities with tissues, like adipose, that can supply fuel molecules. In the case of intermittent parathyroid hormone treatment (PTH), a strategy used to reduce fracture risk, bone formation is proceeded by a change in lipid homeostasis. To investigate the requirement for fatty acid oxidation by osteoblasts during PTH-induced bone formation, we subjected mice with osteoblast-specific deficiency of mitochondrial long-chain b-oxidation as well as mice with adipocyte-specific deficiency for the PTH receptor or adipose triglyceride lipase to an anabolic treatment regime. PTH increased b-oxidation by osteoblasts and the release of fatty acids from adipocytes, while the genetic mouse models were resistant to the hormone’s anabolic effect. Collectively, these data suggest that PTH’s anabolic actions requires coordinated signaling in bone as well as in adipose, wherein a lipolytic response liberates fatty acids that are oxidized by osteoblasts to fuel bone formation