<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Chen Menahem</submitter><instrument_platform>Illumina NovaSeq X</instrument_platform><study_type>RNA-seq of coding RNA</study_type><organism>Rattus norvegicus</organism><species>Rattus norvegicus</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16246</full_dataset_link><description>Growth failure is a major complication of pediatric inflammatory bowel disease (IBD), a condition whose prevalence has risen sharply over recent decades. Despite advances in medical therapy, linear growth impairment often persists. This underscores the urgent need to elucidate how chronic inflammation disrupts skeletal development at the epiphyseal growth plate (EGP), the central driver of longitudinal bone growth. Our study proposes a novel mechanism, involving the activation of ELANE, a serine proteinase previously shown to be secreted by neutrophils in response to inflammatory stimuli. We report for the first time that EGP chondrocytes express ELANE, with significant upregulation observed in DSS-induced colitis and in ATDC5 cells exposed to LPS. The concomitant induction of ELANE and MMP13 indicates a direct catabolic effect on the extracellular matrix, leading to impaired growth plate function. While ELANE is well established in cartilage degradation and bone remodeling in rheumatoid arthritis and osteoarthritis, its expression in the EGP and its role in growth impairment during IBD represent novel findings. These findings open new perspectives on inflammation-driven growth impairment in pediatric IBD, highlight ELANE as a promising therapeutic target to preserve skeletal development.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Nucleic Acid Extraction - RNA was extracted using QIAGEN mirNeasy RNA extraction kit</sample_protocol><sample_protocol>Library Construction - Poly-A/T stretches and Illumina adapters were trimmed from the reads using cutadapt [6]; resulting reads shorter than 30bp were discarded. Reads were mapped to the RatMine reference genome Rnor_6.0 using STAR [2], supplied with gene annotations downloaded from Ensembl (and with EndToEnd option and outFilterMismatchNoverLmax was set to 0.04). Reads with the same UMI were removed using the PICARD MarkDuplicate tool using the BARCODE_TAG parameter. Expression levels for each gene were quantified using htseq-count [3], using the gtf above. Differentially expressed genes were identified using DESeq2 [5] with the betaPrior, cooksCutoff and independentFiltering parameters set to False. Raw P values were adjusted for multiple testing using the procedure of Benjamini and Hochberg. Pipeline was run using snakemake [4]</sample_protocol><sample_protocol>Sample Collection - Epiphyseal growth plates were acquired from young male rats following a DSS induced colitis model. Rats were euthanized and then EGPs were sterility scraped from bone.</sample_protocol><sample_protocol>Sequencing - equencing Libraries were prepared using INCPM mRNAseq. SE reads were sequenced on 2 lane(s) of an Illumina NovaSeq/NextSeq. The output was ~34 million reads per sample.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>Chen Menahem</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA-Seq data from epiphyseal growth plates of young male rats, healthy control rats and dextran sodium sulfate (DSS) induced colitis treated rats</name><description>Growth failure is a major complication of pediatric inflammatory bowel disease (IBD), a condition whose prevalence has risen sharply over recent decades. Despite advances in medical therapy, linear growth impairment often persists. This underscores the urgent need to elucidate how chronic inflammation disrupts skeletal development at the epiphyseal growth plate (EGP), the central driver of longitudinal bone growth. Our study proposes a novel mechanism, involving the activation of ELANE, a serine proteinase previously shown to be secreted by neutrophils in response to inflammatory stimuli. We report for the first time that EGP chondrocytes express ELANE, with significant upregulation observed in DSS-induced colitis and in ATDC5 cells exposed to LPS. The concomitant induction of ELANE and MMP13 indicates a direct catabolic effect on the extracellular matrix, leading to impaired growth plate function. While ELANE is well established in cartilage degradation and bone remodeling in rheumatoid arthritis and osteoarthritis, its expression in the EGP and its role in growth impairment during IBD represent novel findings. These findings open new perspectives on inflammation-driven growth impairment in pediatric IBD, highlight ELANE as a promising therapeutic target to preserve skeletal development.</description><dates><release>2025-11-29T00:00:00Z</release><modification>2025-11-29T18:41:19.569Z</modification><creation>2025-11-21T10:46:04.272Z</creation></dates><accession>E-MTAB-16246</accession><cross_references><ENA>ERP185465</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>