Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Different expression profiles of lncRNAs, mRNAs and circRNAs in degenerative and healthy cervical cartilage endplate (ceRNA)

ABSTRACT: The degeneration of cartilage endplate in cervical disc is considered as a basis of cervical spondylosis. Owing to the important role of post-transcriptional gene regulation in phenotypes and functions of cells, non-coding ribonucleic acid (ncRNA) molecules contributed to the regulation.Degenerated cervical vertebral endplate cartilage specimens were collected from patients with cervical intervertebral disc degeneration (CIDD) that suffered from cervical spondylosis myelopathy, who had received anterior cervical discectomy and fusion (ACDF). CE specimens of healthy subjects were obtained from patients with a cervical fracture who received ACDF at The Second Affiliated Hospital of Nanchang University (Nanchang, China) and adopted SBC human ceRNA array V1.0（4×180K）. The results revealed that expressions of369 lncRNAs, 246 mRNAs, 578 circRNAs were different between degenerated cartilage endplate and healthy cartilage endplate. The functions of differentially expressed lncRNAs and co-expressed potential targeting genes were predicted by analyzing Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathway analysis. Furthermore, we analyzed and find the co-expression and interaction patterns of different RNAs and possible ceRNA mechanism. The present study provided a systematic perspective on the potential function of non-coding RNAs (ncRNAs) in the degeneration of cartilage endplate in CIDD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE153761 | GEO | 2020/07/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression and alternative splicing data from human cartilage endplate-derived stem cells

Project description:Low back pain (LBP) is one of the most prevalent conditions which need medical advice and result in chronic disabilities. Degenerative disc disease (DDD) is a common reason for LBP. A lot of researchers think that CEP degeneration play critical roles in the initiation and development of DDD. In recent years, researchers have put interests on cell-based therapies for regenerating disc structure and function. Our research team has isolated cartilage endplate-derived stem cells (CESCs) and validated their chondrogenic and osteogenic differentiation ability. Enhanced chondrogenic differentiation and inhibited osteogenic differentiation of CESCs may retard CEP calcification and restore the nutrition supply, possibly regenerating the degenerated discs. We used Affymetrix Human Transcriptome Array 2.0 to study the global gene expression profilling and alternative splicing events during the chondrogenic and osteogenic differentiation of cartilage endplate-derived stem cells. The cartilage endplate-derived stem cells(CESCs) were induced to undergo chondrogenic(CD) and osteogenic differentiation(OD). Both undifferentiated and differentiated CESCs were sent for RNA extraction and hybridization on Affymetrix microarrays. A comparative analysis was done between the undifferentiated and differentiated samples.

2015-12-21 | E-GEOD-63897 | biostudies-arrayexpress

Gene expression and alternative splicing data from human cartilage endplate-derived stem cells

2015-12-21 | GSE63897 | GEO

Different expression profiles of lncRNAs, mRNAs and circRNAs in degenerative and healthy cervical cartilage endplate (ceRNA)

Project description:Different expression profiles of lncRNAs, mRNAs and circRNAs in degenerative and healthy cervical cartilage endplate (ceRNA)

| PRJNA643990 | ENA

Expression and alternative splicing data of cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

Project description:Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could influence the fate of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) of CESCs under hypoxia compared to those under normoxia. Human cartilage endplate-derived stem cells (CESCs) were cultured under normoxia and hypoxia for 21 days respectively.

2016-07-18 | E-GEOD-84484 | biostudies-arrayexpress

Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

Project description:Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) during osteogenic differentiation of CESCs under hypoxia compared to those induced under normoxia. Human cartilage endplate-derived stem cells (CESCs) were treated with osteogenic differentiation medium under normoxia and hypoxia for 21 days respectively.

2016-06-14 | E-GEOD-83284 | biostudies-arrayexpress

Expression and alternative splicing data of cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

2016-07-18 | GSE84484 | GEO

Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

Project description:Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) during osteogenic differentiation of CESCs under hypoxia compared to those induced under normoxia.

2016-06-14 | GSE83284 | GEO

Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

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

microRNA expression in facet cartilage degeneration

Project description:Osteoarthritis (OA) of spine (facet joints; FJ) is one of the major causes of severe low back pain and disability worldwide. The degeneration of facet cartilage is a hallmark of FJ OA. However, endogenous mechanisms that initiate degeneration of facet cartilage are unknown and there are no disease-modifying therapies to stop FJ OA. In this study we performed microRNA array analysis to identify differentially expressed microRNAs in facet cartilage from patients with FJ OA compared to facet cartilage from patients with lumbar disc herniation (LDH).

2016-03-15 | GSE79258 | GEO

The degradome of the human intervertebral disc

Project description:The intervertebral disc (IVD) is a joint in the spine that facilitates daily physical activity, comprising of the central nucleus pulposus (NP), surrounded by the annulus fibrosus (AF) and sandwiched between two cartilage endplates that function together as a unit. Changes to the IVD occur with aging, most drastically in the NP where it experiences dehydration and loss of cellularity, directly impacting on the integrity of the biomechanical functions of the IVD. We were interested in examining the types of degraded proteins in young and aged disc samples to further understand the protein turnover in aging and homeostasis. We analysed the degradome for degraded proteins using terminal amine isotopic labeling of substrates (TAILS) Clinical specimens from spine surgeries for scoliosis (young samples, n=3) or degeneration (aged samples, n=3) were used in this study.

2021-01-29 | PXD018298 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data