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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [RNA-seq]

ABSTRACT: Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [RNA-seq]

PROVIDER: PRJNA975172 | ENA |

REPOSITORIES: ENA

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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation

Project description:Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation

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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [ChIP-Seq]

Project description:Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [ChIP-Seq]

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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [ChIP-Seq]

Project description:After preliminary verification of physical interaction between PTH1R and THR, we next performed chromatin co-immunoprecipitation sequencing (ChIP -seq) to detect the overlapping downstream promoters genome-widely between PTH1R and THR.

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Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [RNA-seq]

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Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

Project description:To investigation the role of PTH and Kindlin-2 in bone development, we performed single-cell RNA-sequencing. From Con-veh, Con-PTH, cKO-veh, cKO-PTH, we profiled more than 20k single cells, including multi-potent mesenchymal stromal cells (MSC), osteoprogenitors, osteoblasts, chondrocytes, fibroblasts, endothelial cells, smooth muscle cells, skeletal muscle cells, pericytes, and schwann cells. We found proportion of part of these cells were significant altered by PTH or Kindlin-2 loss, especially for MSC, osteoblast, chondrocyte, and fibroblast. Transcriptomic analysis revealed gene expression was dramatically regulated by PTH or Kindlin-2 loss.

2020-10-01 | GSE150291 | GEO

Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

Project description:Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

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The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH

Project description:Glucocorticoids (GC) and parathyroid hormone (PTH) are widely used therapeutic endocrine hormones where their effects on bone and joint arise from actions on multiple skeletal cell types. In osteocytes, GC and PTH exert opposing effects on perilacunar canalicular remodeling (PLR). Suppressed PLR can impair bone quality and joint homeostasis, including in GC-induced osteonecrosis. However, combined effects of GC and PTH on PLR are unknown. Focusing on subchondral bone and joint homeostasis, we hypothesize that PTH, a PLR agonist, could rescue GC-suppressed PLR. The skeletal effects of GC and PTH, alone or combined, were examined in male and female mice by micro-computed tomography, mechanical testing, histology, and gene expression analysis. For each outcome, females were more responsive to GC and PTH than males. GC and PTH exerted regional differences, with GC increasing trabecular bone volume but reducing cortical bone thickness, stiffness, and ultimate force. Despite PTH’s anabolic effects on trabecular bone, it did not rescue GC’s catabolic effects on cortical bone. Likewise, cartilage integrity and subchondral bone apoptosis, alkaline phosphatase activity, and osteocyte lacunocanalicular networks showed no evidence that PTH could offset GC-dependent effects. Rather, GC and PTH each increased cortical bone gene expression implicated in bone resorption by osteoclasts and osteocytes, including Acp5, Mmp13, Atp6v0d2, Ctsk, differences maintained when GC and PTH were combined. Since PTH is insufficient to rescue GC’s effects on young female mouse bone, future studies are needed to determine if osteocyte PLR suppression, due to GC, aging, or other factors, can be offset by a PLR agonist.

2024-07-18 | GSE252085 | GEO

Gene expression in human breast cancer T47D cells associated with expression of PTH-AS, a lncRNA downstream of parathyroid hormone

Project description:To comprehensively analyze the effect of PTH-AS on gene expression, microarray analysis was performed using human breast cancer T47D cells expressing PTH-AS. The gene expression levels of full-length PTH-AS expressing T47D cells (T47D-PA6) and vector control (T47D-VC1) or incomplete PTH-AS expressing T47D cells (T47D-PA5) were compared. As a result, 1453 genes were differentially expressed in his T47D-PA6 compared to T47D-VC1. Except for genes whose expression was altered in T47D-PA5 cells expressing incomplete PTH-AS, PTH-AS expression in T47D cells upregulated 914 genes and downregulated 600 genes. Many of the altered genes have been classified as immune-related biological processes. Particularly striking was the significant upregulation of JAK-STAT pathway-related genes, including the interferon-related DNA damage resistance signature (IRDS) that promotes cancer.

2022-05-21 | GSE176467 | GEO

Expression data from placenta harvested from WT and Pth-null fetuses treated 90 minutes prior with saline or PTH (1-84)

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.

2010-03-01 | GSE16983 | GEO

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