Effect of Glucocorticoids on lncRNA and mRNA Expression Profiles of the Human Bone Microcirculatory Endothelial Cells from Femoral Head
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE60332 | GEO | 2015/01/01
SECONDARY ACCESSION(S): PRJNA258051
REPOSITORIES: GEO
Similar Datasets
Project description:Appropriate gene expression patterns form the basis for bone microcirculatory endothelial cellsM-bM-^@M-^Y function and bone morphology. Although previous studies have elucidated the impact of hydrocortisone on bone microcirculatory endothelial cellsM-bM-^@M-^Y specific gene expression, the exact differential transcriptomes and comprehensive gene expression profiles remain unknown. We have investigated the mRNA and lncRNA expression patterns before and after hydrocortisone administration of bone microcirculatory endothelial cells. At mRNAs level totally 518 differentially expressed genes were identified. Furthermore, we identified 73 upregulated and 166 downregulated long non-coding RNAs after administration of hydrocortisone. These RNAs appeared to be highly important to gene co-expression network. Transcriptomic analysis of bone microcirculatory endothelial cells from human samples is highly informative due to their relevance to the large number of expressed genes. Our study provides a very valuable basis for investigation of genes, regulation and their co-expression network contributing to hydrocortisone induced disorders. Two-condition experiment, hydrocortisone treated vs. untreated bone microcirculatory endothelial cells. Biological replicates: 8 control replicates, 8 treated replicates.
2015-01-01 | E-GEOD-60332 | biostudies-arrayexpress
Project description:Appropriate gene expression patterns form the basis for bone microcirculatory endothelial cells’ function and bone morphology. Although previous studies have elucidated the impact of hydrocortisone on bone microcirculatory endothelial cells’ specific gene expression, the exact differential transcriptomes and comprehensive gene expression profiles remain unknown. We have investigated the microRNA expression patterns before and after hydrocortisone administration of bone microcirculatory endothelial cells. Only 5 microRNAs were Benjamini-Hochberg characterized over 368 microRNAs candidates. Transcriptomic analysis of bone microcirculatory endothelial cells from human samples is highly informative due to their relevance to the large number of expressed genes. Our study provides a very valuable basis for investigation of genes, regulation and their co-expression network contributing to hydrocortisone induced disorders.
2015-01-01 | GSE60093 | GEO
Project description:Rationale: Despite shortening vasopressor use in shock, hydrocortisone administration remains controversial, with potential harm on the immune system. Few studies assessed hydrocortisone impact on the transcriptional response in shock, and we are lacking data in burns. Objectives: To assess the hydrocortisone-induced transcriptional modulation in severe burn shock, particularly on the immune response. Methods: We collected whole blood samples (n= 117) during a randomized controlled trial assessing the efficacy of hydrocortisone administration on burn shock. Using whole genome microarrays, we first compared burn patients from the placebo group (n=15) to healthy volunteers (n=13) to describe the transcriptional modulation induced by burn shock over the first week. Then we compared burn patients randomized for either hydrocortisone administration (n=15) or placebo (n=15) to assess hydrocortisone-induced modulation. Measurements and Main Results: Study groups were similar in terms of severity and major outcomes, but shock duration (significantly reduced in the hydrocortisone group). Many genes (n=2250) were differentially expressed between burn patients and healthy volunteers, with 85% of them exhibiting a profound and persistent modulation over seven days. Interestingly, we showed that hydrocortisone enhanced the shock-associated repression of adaptive, but also innate immunity. Conclusions: We found that the initial host response to burn shock encompasses a wide and persistent modulation of gene expression, with profound modulation of pathways associated with metabolism and immunity. Importantly, hydrocortisone administration may worsen the immunosuppression associated with severe injury. These data should be taken into account in the risk ratio of hydrocortisone administration in patients with inflammatory shock.
2017-07-02 | GSE77791 | GEO
Project description:The homeostasis of bone metabolism depends on the coupling and precise regulation of various types of cells in bone tissue. However, the communication and interaction between bone tissue cells at the single-cell level remains poorly understood. Thus, we performed single-cell RNA sequencing (scRNA-seq) on the primary human femoral head tissue cells (FHTCs). Nine cell types were identified in 26,574 primary human (FHTCs), including granulocytes, T cells, monocytes, B cells, red blood cells, osteoblastic lineage cells, endothelial cells, endothelial progenitor cells (EPCs) and plasmacytoid dendritic cells. We identified serine protease 23 (PRSS23) and matrix remodeling associated protein 8 (MXRA8) as novel bone metabolism-related genes. Additionally, we found that several subtypes of monocytes, T cells and B cells were related to bone metabolism. Cell-cell communication analysis showed that collagen, chemokine, transforming growth factor and their ligands have significant roles in the crosstalks between FHTCs. In particular, EPCs communicated with osteoblastic lineage cells closely via the "COL2A1-ITGB1" pair. Collectively, this study provided an initial characterization of the cellular composition of the human FHTCs and the complex crosstalks between them at the single-cell level. It is a unique starting resource for in-depth insights into bone metabolism.
2021-03-24 | GSE169396 | GEO
Project description:Expression quantitative trait locus (QTL) mapping of 127 adult femoral bone samples from a Red Junglefowl x White Leghorn advanced intercross line. Bone trait QTL have been mapped in the same cross, allowing a genetical genomics approach to quantitative trait gene identification
2015-10-31 | E-MTAB-3141 | biostudies-arrayexpress
Project description:The steriod-induced necrosis of femoral head(SINFH) is a serious clinical problem and the underlying mechanism of this disease remains unknown. As its etiology and pathogenesis are not clear, there hasn’t been an effective treatment yet. In-depth studies on its pathogenesis will provide important information for the prevention and treatment of this devastated disease. Animal model researches are helpful to a better understanding of its etiology and pathogenesis, to early diagnosis and treatments and provide the basis for clinical treatment It has been proved that the occurrence of SINFH is related to gene itself and its polymorphism. These studies, in which only one or a few genes were investigated, could not provide a comprehensive understanding to the pathogenesis of SINFH. We used microarrays to compare the gene expression profile of SINFH rats with that of normal rats and identified gene expression changes between SINFH rats and normal rats. Adult healthy male Wistar rats(body weight 200±10g) were randomly divided into control and experimental groups. All the rats were given injection of E. coli endotoxin at a dose of 20μg/kg body weight into abdominal cavity for two times with a 24 hour interval. 24 hours after the second administration of E. coli endotoxin, methylprednisolone 40mg/kg was administered into the left gluteus muscle of experimental group rats for three times with a 24 hour interval. Rats were then killed 6 weeks after steroid administration. In experiment, immediately after death the left femoral heads were isolated. Femoral heads were used for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the gene expression profile of SINFH rats and that of normal rats in order to identified gene expression changes between SINFH rats and normal rats by comparing the gene expression profile of SINFH rats with that of normal rats. To that end, we have established the gene expression profiles of normal and SINFH disease of rat femoral head and found out differentially expressed genes.
2010-12-28 | E-GEOD-26316 | biostudies-arrayexpress
Project description:Endothelial cells play a critical role in multiple cardiovascular diseases. CD34+ cells are believed to be endothelial progenitors that have been used to treat cardiovascular disease. However, the exact identity and the role of CD34+ cells in vascular regeneration remains unclear.Here we performed single cell RNA sequencing to identify heterogeneous CD34+ cells serve as a contributor to endothelial regeneration.
2021-10-13 | GSE182232 | GEO
Project description:Lameness due to femoral head separation (FHS) is a production and welfare issue in commercial poultry. FHS is an idiopathic disorder, which is attributed to a myriad of factors but in order to improve bone health, broiler breeders must be prognosed for disease susceptibility and selected against FHS using biomarkers. Proteins from plasma of blood, which can be obtained using minimally invasive methods represent an ideal, rich source of biomarkers which might be different in susceptible or affected birds. The peptide and proteins in plasma of healthy (HLTH) and affected birds (FHS) were compared using Matrix assisted laser desorption ionization mass spectrometry (MALDI-TOF-MS) and Liquid chromatography and tandem mass spectrometry (LC-MS/MS). The peptide profile of HLTH and FHS were compared using ClinPro tools and the differentially expressed peptides were isolated by Reverse phase liquid chromatography fractionation (C18-RP-HPLC) and identified using peptide mass fingerprinting. Peptides derived from fibrinogen precursor and fetuin were reduced in FHS birds. Based on the proteomic analysis, proteins such as Gallinacin 10, Apolipoprotein A-1 and Hemoglobin chains are elevated in FHS while Alpha 1-acid glycoprotein is reduced in FHS birds. Our study shows that bodyweight, lipid profile and the above mentioned proteins could be useful as a biomarker for improvement of bone health. These proteins indicate that blood lysis, antimicrobial defense and lipid disorder but lack of an inflammatory response might be consequential to FHS.
2016-08-09 | PXD003292 | Pride
Project description:The cartilage degeneration that accompanies subchondral bone necrosis plays an important role in the development of osteonecrosis of femoral head (ONFH). To better understand the molecular basis of cartilage degradation in ONFH, we compared the proteomics profile of ONFH cartilage with that of normal controls
2021-01-20 | PXD023698 |
Project description:This a model from the article:
Parathyroid hormone temporal effects on bone formation and resorption.
Kroll MH. Bull Math Biol
2000 Jan;62(1):163-88 10824426
,
Abstract:
Parathyroid hormone (PTH) paradoxically causes net bone loss (resorption) when
administered in a continuous fashion, and net bone formation (deposition) when
administered intermittently. Currently no pharmacological formulations are
available to promote bone formation, as needed for the treatment of
osteoporosis. The paradoxical behavior of PTH confuses endocrinologists, thus, a
model bone resorption or deposition dependent on the timing of PTH
administration would de-mystify this behavior and provide the basis for logical
drug formulation. We developed a mathematical model that accounts for net bone
loss with continuous PTH administration and net bone formation with intermittent
PTH administration, based on the differential effects of PTH on the osteoblastic
and osteoclastic populations of cells. Bone, being a major reservoir of body
calcium, is under the hormonal control of PTH. The overall effect of PTH is to
raise plasma levels of calcium, partly through bone resorption. Osteoclasts
resorb bone and liberate calcium, but they lack receptors for PTH. The
preosteoblastic precursors and preosteoblasts possess receptors for PTH, upon
which the hormone induces differentiation from the precursor to preosteoblast
and from the preosteoblast to the osteoblast. The osteoblasts generate IL-6;
IL-6 stimulates preosteoclasts to differentiate into osteoclasts. We developed a
mathematical model for the differentiation of osteoblastic and osteoclastic
populations in bone, using a delay time of 1 hour for differentiation of
preosteoblastic precursors into preosteoblasts and 2 hours for the
differentiation of preosteoblasts into osteoblasts. The ratio of the number of
osteoblasts to osteoclasts indicates the net effect of PTH on bone resorption
and deposition; the timing of events producing the maximum ratio would induce
net bone deposition. When PTH is pulsed with a frequency of every hour, the
preosteoblastic population rises and decreases in nearly a symmetric pattern,
with 3.9 peaks every 24 hours, and 4.0 peaks every 24 hours when PTH is
administered every 6 hours. Thus, the preosteoblast and osteoblast frequency
depends more on the nearly constant value of the PTH, rather than on the
frequency of the PTH pulsations. Increasing the time delay gradually increases
the mean value for the number of osteoblasts. The osteoblastic population
oscillates for all intermittent administrations of PTH and even when the PTH
infusion is constant. The maximum ratio of osteoblasts to osteoclasts occurs
when PTH is administered in pulses of every 6 hours. The delay features in the
model bear most of the responsibility for the occurrence of these oscillations,
because without the delay and in the presence of constant PTH infusions, no
oscillations occur. However, with a delay, under constant PTH infusions, the
model generates oscillations. The osteoblast oscillations express limit cycle
behavior. Phase plane analysis show simple and complex attractors. Subsequent to
a disturbance in the number of osteoblasts, the osteoblasts quickly regain their
oscillatory behavior and cycle back to the original attractor, typical of limit
cycle behavior. Further, because the model was constructed with dissipative and
nonlinear features, one would expect ensuing oscillations to show limit cycle
behavior. The results from our model, increased bone deposition with
intermittent PTH administration and increased bone resorption with constant PTH
administration, conforms with experimental observations and with an accepted
explanation for osteoporosis.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Kroll MH. (2000) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230083 | BioModels