Gene expression in murine cartilage, 3 months of age, wild type vs miR-455 null
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1146336 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30184267_1.fastq.gz | Fastqsanger.gz | |||
| SRR30184267_2.fastq.gz | Fastqsanger.gz | |||
| SRR30184268_1.fastq.gz | Fastqsanger.gz | |||
| SRR30184268_2.fastq.gz | Fastqsanger.gz | |||
| SRR30184269_1.fastq.gz | Fastqsanger.gz |
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Project description:MicroRNA-455 is a key microRNA in cartilage, strongly induced by Sox9. Using CrispR-Cas9, we produced a global deletion of miR-455 in the mouse and characterised cartilage and bone. In this study, we compared the cartilage gene expression in 3 month old mice, between wild-type and miR-455 null.
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Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride
Project description:MicroRNA-455 is a key microRNA in cartilage, strongly induced by Sox9. In order to understand its function, we have overexpressed (miR-455-3p mimic) or inhibited (miR-455-3p inhibitor) miR-455 compared to appropriate controls and measured gene expression.
2025-02-26 | GSE276347 | GEO
Project description:MicroRNA-455 is a key microRNA in cartilage, strongly induced by Sox9. Overexpression of miR-455-3p in the developing chick limb bud at HH18-19 causes a reduction in limb bud size at HH24-25.
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Project description:Coemansia sp. RSA 455 Resequencing
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Project description:Regulation between the fed and fasted state in mammals is partially controlled by peroxisome proliferator activated receptor-alpha (PPAR-alpha). Expression of the receptor is high in liver, heart and skeletal muscle, but decreases with age. A combined 1H NMR spectroscopy and GC-MS metabolomic approach has been used to examine metabolism in liver, heart, skeletal muscle and adipose tissue in PPAR-alpha null mice and wild type controls during ageing between 3-13 months. For the PPAR-alpha-null mouse multivariate statistics highlighted hepatic steatosis, reductions in the concentrations of glucose and glycogen in both liver and muscle tissue, and profound changes in lipid metabolism in each tissue, reflecting known expression targets of the PPAR-alpha receptor. Hepatic glycogen and glucose also decreased with age for both genotypes. These findings indicate the development of age related hepatic steatosis in the PPAR-alpha-null mouse, with the normal metabolic changes associated with ageing exacerbating changes associated with genotype. Furthermore, the combined metabolomic and multivariate statistics approach provides a robust method for examining the interaction between age and genotype. </p> The GC-MS assay for this study can be found in the MetaboLights study MTBLS314.
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Project description:Hui2014 - Age-related changes in articular
cartilage
This model is described in the article:
Oxidative changes and
signalling pathways are pivotal in initiating age-related
changes in articular cartilage
Wang Hui1, David A Young1, Andrew D
Rowan1, Xin Xu2, Tim E Cawston1, Carole J Proctor1,3
Annals of the Rheumatic Diseases
Abstract:
Objective: To use a computational approach to investigate
the cellular and extracellular matrix changes that occur with
age in the knee joints of mice. Methods: Knee joints from an
inbred C57/BL1/6 (ICRFa) mouse colony were harvested at
3–30?months of age. Sections were stained with H&E,
Safranin-O, Picro-sirius red and antibodies to matrix
metalloproteinase-13 (MMP-13), nitrotyrosine, LC-3B, Bcl-2, and
cleaved type II collagen used for immunohistochemistry. Based
on this and other data from the literature, a computer
simulation model was built using the Systems Biology Markup
Language using an iterative approach of data analysis and
modelling. Individual parameters were subsequently altered to
assess their effect on the model. Results: A progressive loss
of cartilage matrix occurred with age. Nitrotyrosine, MMP-13
and anaplastic lymphoma kinase (ALK1) staining in cartilage
increased with age with a concomitant decrease in LC-3B and
Bcl-2. Stochastic simulations from the computational model
showed a good agreement with these data, once transforming
growth factor-? signalling via ALK1/ALK5 receptors was
included. Oxidative stress and the interleukin 1 pathway were
identified as key factors in driving the cartilage breakdown
associated with ageing. Conclusions: A progressive loss of
cartilage matrix and cellularity occurs with age. This is
accompanied with increased levels of oxidative stress,
apoptosis and MMP-13 and a decrease in chondrocyte autophagy.
These changes explain the marked predisposition of joints to
develop osteoarthritis with age. Computational modelling
provides useful insights into the underlying mechanisms
involved in age-related changes in musculoskeletal tissues.
This model is hosted on
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2024-09-02 | BIOMD0000000560 | BioModels
Project description:MiR-455-3p has been reported to suppress the expression of ROCK2, HOXB5, hTERT, and RUNX2, which are involved in multiple biological processes including renal fibrosis, chondrogenic development and differentiation, Alzheimer’s disease, preeclampsia, and tumorigenesis. Here, we showed that miR-455-3p broadly inhibited TGF-beta-induced EMT by repressing the expression of Smad2, ZEB1, and HDAC2 in breast cancer cells, and that miR-455-3p loss-of-function promotes the acquisition of cell invasive properties and the ability to metastasize. These results indicate that miR-455-3p represents an important node that inhibits metastasis of breast cancer.
2019-09-06 | GSE129146 | GEO
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