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Effect of Parathyroid Hormone Analog Treatment on Gene Expression

ABSTRACT: Effect of Parathyroid Hormone Analog Treatment on Gene Expression

PROVIDER: PRJNA751605 | ENA |

REPOSITORIES: ENA

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Effect of Parathyroid Hormone Analog Treatment on Gene Expression

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.

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Parathyroid Hormone Treatment Effect on Gene Expression in Primary Calvarial Osteoblasts

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Parathyroid Hormone Treatment Effect on Gene Expression in Primary Calvarial Osteoblasts

Project description:Parathyroid Hormone Treatment Effect on Gene Expression in Primary Calvarial Osteoblasts

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Parathyroid hormone exacerbates pulmonary hypertension through hypoxia-induced parathyroid hormone receptor upregulation.

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.

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Parathyroid hormone exacerbates pulmonary hypertension through hypoxia-induced parathyroid hormone receptor upregulation.

Project description:Parathyroid hormone exacerbates pulmonary hypertension through hypoxia-induced parathyroid hormone receptor upregulation.

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Transcription profiling of mouse primary osteoblastic cells after intermittent of continuous treatment with parathyroid hormone to investigate the role of beta-arrestin2

Project description:Role of beta-arrestin2 in response to intermittent or continuous parathyroid hormone (PTH) treatment.

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Project description:The aim of this study was to explore the involvement of long noncoding RNAs (lncRNAs) during intermittent parathyroid hormone (PTH) induced cementogenesis.

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Disintegrin-and-metalloproteinase-19 cleaves parathyroid hormone receptor and could cause brachydactyly type E

Project description:Brachydactyly type E (BDE), shortened metacarpals, metatarsals, cone-shaped epiphyses, and short stature, is an autosomal-dominant condition that commonly occurs as a sole phenotype. Parathyroid hormone-like protein (PTHrP) has been shown to be responsible in all forms to date, either directly or indirectly. We used linkage and then whole genome sequencing in a small pedigree, to elucidate BDE and identified a truncated disintegrin-and-metalloproteinase-19 (ADAM19) allele in all affected family members, but not in nonaffected persons. Since we had shown earlier that the extracellular domain of the parathyroid hormone receptor (PTHR1) is subject to an unidentified metalloproteinase cleavage, we tested the hypothesis that ADAM19 is a sheddase for PTHR1. Wild-type ADAM19 cleaved PTHR1, while mutated ADAM-19 did not. Alanine substitutions mapped the N-terminal cleavage site of PTHR1. For mass spectrometry verification, different proteases have been used, to identify the cleavage products in ADAM-19 and PTHR1 transfected HEK-293 cells.

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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

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