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Different expression of circRNAs in blood from idiopathic short stature patients and healthy controls

ABSTRACT: Different expression of circRNAs in blood from idiopathic short stature patients and healthy controls

PROVIDER: PRJNA660266 | ENA |

REPOSITORIES: ENA

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Different expression of circRNAs in blood from idiopathic short stature patients and healthy controls

Project description:Idiopathic short stature is diagnosed by a standing height of less than two standard deviation scores in a specific population adjusted for age and gender and the exclusion of identifiable diseases. A series of studies have confirmed that noncoding RNAs can regulate the chondrocyte proliferation, hypertrophy, and endochondral ossification in the growth plate. In order to analyze and find differentially expressed circRNAs in Idiopathic short stature and healthy controls, we aimed to explore whether differentially expressed circRNAs in idiopathic short stature. Four pairs of blood samples were subjected to microarray analysis using the Arraystar Human CircRNAs Microarray v2 (Arraystar, USA). Compared to normal individuals, in ISS patients, the expression levels of 83 circRNAs were upregulated and those of 62 were downregulated.

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Different expression of ceRNAs (lncRNAs, circRNAs and mRNAs) in peripheral blood exosomes from idiopathic short stature patients and healthy controls

Project description:Idiopathic short stature is diagnosed by a standing height of less than two standard deviation scores in a specific population adjusted for age and gender and the exclusion of identifiable diseases. A series of studies have confirmed that noncoding RNAs can regulate the chondrocyte proliferation, hypertrophy, and endochondral ossification in the growth plate. In order to analyze and find differentially expressed ceRNAs (lncRNAs, circRNAs and mRNAs in peripheral blood exosomes of idiopathic short stature and healthy controls, we aimed to explore whether differentially expressed ceRNAs (lncRNAs, circRNAs and mRNAs) in peripheral blood exosomes of idiopathic short stature. Three pairs of peripheral blood exosomes samples were subjected to microarray analysis using the SBC human ceRNA Microarray.

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DNA methylation sequencing of SLC22A18 between short stature patients and controls

Project description:We found the expression of SLC22A18 in short stature patients is lower than that in controls by qPCR. DNA methylation is one of the most possible reason to make the expression of SLC22A18 abnormal. So we quantified the promoter methylation levels of 3 patients and 3 healthy controls by deep sequencing.

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Project description:Case series of children and adolescents undergoing growth hormone stimulation testing for investigation of short stature. The aim of this study was to identify whether a machine learning approach utilising gene expression data could predict which short children would test positive for GHD and which would not.

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Short Stature, GH stimulation testing and RNASeq

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DNA methylation sequencing of SLC22A18 between short stature patients and controls

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Project description:It is important to access whether growth hormone (GH) is capable of producing its own epigenetic marks on the methylome. We aim to perform a comprehensive pharmaco-epigenomics analysis of DNA methylation changes on responding to long-term GH treatment in children with idiopathic short stature. We measured DNA methylation profiles before and after GH treatment (with a duration of aprox18 months in average) on 49 healthy children using customized methylC-seq capture sequencing.

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Profiling of upstream enhancers of SHOX in idiopathic short stature and functional characterization of the cis-regulatory landscape of SHOX

Project description:SHOX mutations and deletions of the downstream regulatory region have been reported in cases with idiopathic short stature (ISS) and Leri-Weill dyschondrosteosis (LWD). Recently, a deletion and duplication of upstream enhancers have been described in ISS. Here, we aimed to evaluate the contribution of upstream copy number variations (CNVs) to the pathogenesis of ISS, to validate the enhancer role of the upstream enhancers in human cells, and to characterize the chromatin architecture of the cis-regulatory landscape of SHOX. CNV analysis of three upstream conserved non-coding elements (CNEs), CNE-5, CNE-3 and CNE-2, in 501 ISS referrals with no established molecular diagnosis revealed two deletions and one duplication. Enhancer activity of the upstream CNEs was corroborated by luciferase assays in human osteosarcoma U2OS cells. In addition, all three CNEs overlap with reported H3K27ac ChIP-seq marks in human embryonic limb buds. To characterize the chromatin interaction profile of the SHOX region, chromosome conformation capture (4C-seq) was performed in chicken embryo limb buds and in U2OS cells, revealing interactions of the upstream CNEs with the SHOX promoter. Moreover, the 4C-seq interaction maps and H3K27ac marks indicated that the cis-regulatory landscape of SHOX encompasses 1 Mb, suggesting additional cis-regulatory elements controlling SHOX.In conclusion, we showed that upstream CNVs of SHOX are rare in ISS and have incomplete penetrance. Chromatin interaction maps, luciferase assays and H3K27ac marks further support an enhancer function for the upstream CNEs. Finally, we demonstrated that the cis-regulatory landscape of SHOX is larger than previously anticipated potentially harboring novel cis-regulatory elements, which may be involved in the pathogenesis of molecularly unsolved ISS cases..

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Profiling of upstream enhancers of SHOX in idiopathic short stature and functional characterization of the cis-regulatory landscape of SHOX

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