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Single-cell transcriptomics of human cholesteatoma identifies an activin A-producing osteoclastogenic fibroblast subset inducing bone destruction

ABSTRACT: Single-cell transcriptomics of human cholesteatoma identifies an activin A-producing osteoclastogenic fibroblast subset inducing bone destruction

PROVIDER: PRJNA864843 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20738300_1.fastq.gz	Fastqsanger.gz
	SRR20738300_2.fastq.gz	Fastqsanger.gz
	SRR20738301_1.fastq.gz	Fastqsanger.gz
	SRR20738301_2.fastq.gz	Fastqsanger.gz
	SRR20738296_1.fastq.gz	Fastqsanger.gz

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Single-cell transcriptomics of human cholesteatoma identifies an activin A-producing osteoclastogenic fibroblast subset inducing bone destruction

Project description:To elucidate the mechanism underlying bone erosion in cholesteatoma, we performed scRNA-seq using human cholesteatoma tissues surgically resected from patients. We focused on pathogenic fibroblasts or keratinocytes, and therefore CD45-negative cells were collected for scRNA-seq analysis to exclude hematopoietic cell lineages. As there are no “normal” tissues in the middle ear that correspond to cholesteatoma, retroauricular skin at the incision site was used as the control for analysis of cholesteatoma. We dentified a characteristic pathogenic fibroblast subset with abundant expression of inhibin βA.

2023-05-29 | GSE210261 | GEO

Single-cell transcriptomics of human cholesteatoma identifies an activin A-producing osteoclastogenic fibroblast subset inducing bone destruction.

Project description: Not available

| S-EPMC10400591 | biostudies-literature

Fibroblasts in cholesteatoma activate osteoclasts.

Project description:Cholesteatoma arises from a tympanic membrane and expands in the middle ear. It erodes the surrounding bone and leads to hearing loss or brain abscess which is lethal complication. Currently, the only effective treatment is the complete surgical removal of cholesteatoma. However, possibility of recurrence is not satisfactory, other clinical treatment is desired. A mechanism of bone erosion in rheumatoid arthritis, which is one of the bone destructive disease, is progressing to be clarified. Receptor activator of NF-κB ligand (RANKL) secreted by synovial fibroblasts, T cells, and B cells lead to differentiation and activation of osteoclast precursor in rheumatoid arthritis. In contrast it has been still unclear why cholesteatoma erodes bone. In the current study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. In this study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. We investigated upstream of RANKL from RNA sequence results by Ingenuity Pathways Analysis, which is data base of abundance information about molecular biology.

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Large scale proteomics of cholesteatoma

Project description:The study describes comprehensive proteomics data of the cholesteatoma disease. Cholesteatoma is a serious and destructive growth of keratinizing squamous epithelium in the middle ear, with a poorly understood etiopathogenesis. The large scale proteomics approach used in this study highly expands our molecular knowledge of cholesteatoma and implicates several biological functions in its pathology. Human samples of cholesteatoma, neck of cholesteatoma, tympanic membrane, external auditory canal skin, and middle ear mucosa were analyzed. Approximately two thousand unique proteins were identified by label-free nanoLC-MS/MS proteomics. The protein and peptide identification data were obtained by Proteome Discoverer (Thermo Scientific, version 1.3.0.339) processing of LTQ Orbitrap raw files using the Mascot algorithm (Matrix Sciences, version 2.4.0). To yield comprehensive proteome data the tissue biopsy was separated into ten protein fractions, which were MS analysed separately, and the resulting MS files were subsequently merged in the database analysis. Precursor mass tolerance was 5 ppm and fragment mass tolerance was 0.5 Da. Dynamic Modification was Oxidation (M) and Static Modification was Carbamidomethyl (C); annotated in the PRIDE files as mass deviations (e g for double charged peptides m/z deviation of approximately 8.00 and 28.51 for modification of Met and Cys, respectively). FASTA file was SwissProt_2012_03.fasta (containing 20,255 Homo sapiens sequences). MudPit scoring was applied, and up to two missed trypsin cleavages were accepted. Peptide cut off Score was 10 and protein relevance threshold was 20.

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Identification of Novel Cholesteatoma-related Gene Expression Signatures Using Full-genome Microarrays

Project description:In this study, we investigated differentially expressed genes in human cholesteatomas in comparison to regular auditory canal skin using Whole Human Genome Microarrays that contain 19,596 human genes. In addition to already described up-regulated mRNAs in cholesteatoma, such as MMP9, DEFB2 and KRT19, we identified 3558 new cholesteatoma-related transcripts. 811 genes appear to be significantly differentially up-regulated in cholesteatoma. 334 genes were down-regulated more than 2-fold. Significantly regulated genes with protein metabolism activity include matrix metalloproteinases as well as PI3, SERPINB3 and SERPINB4. Genes like SPP1, KRT6B, PRPH, SPRR1B and LAMC2 are known as genes with cell growth and/or maintenance activity. Transport activity genes and signal transduction genes are LCN2, GJB2 and CEACAM6. The three cell communication genes are CDH19 and genes belonging to the S100 family. Two samples from each patient (cholesteatoma vs. normal auditory canal skin) for each two-colour hybridisation experiment

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Bone Marrow Monocyte/Macrophage Derived Activin A Mediates the Osteoclastogenic Effects of IL-3 in Myeloma

Project description:Myeloma bone disease is characterized by tremendous bone destruction with suppressed bone formation. IL-3 is a multifunctional cytokine that increases myeloma cell growth and osteoclast proliferation while inhibiting osteoblast differentiation. While IL-3 appears to be an attractive therapeutic target for myeloma, attempts at targeting IL-3 have been unsuccessful due to IL-3M-bM-^@M-^Ys effects on normal hematopoiesis. Thus identification of IL-3M-bM-^@M-^Ys downstream effects in MMBD is important for effective targeting of this cytokine in MM. Here we demonstrated that treatment of myeloma patient CD14+ bone marrow monocyte / macrophages with IL-3 induces high levels of Activin A (ActA), a pluripotent TGF-M-NM-2 superfamily member that, like IL-3, modulates MMBD by enhancing osteoclastogenesis and inhibiting osteoblasts. We show that IL-3 induced osteoclastogenesis is mediated by ActA and is RANKL independent. Additionally, IL-3 induced ActA secretion is greatest early in osteoclastogenesis and ActA acts early in osteoclastogenesis. Therefore we suggest that therapies targeting ActA production should block IL-3M-bM-^@M-^Ys effects in myeloma bone disease. Investigate the mediators of IL-3M-bM-^@M-^Ys effects on bone remodeling in myeloma we performed gene expression profiling using Affymetrix GeneChip analysis of IL-3 treated CD14+ peripheral blood from healthy donor.

2014-11-01 | E-GEOD-41992 | biostudies-arrayexpress

N6-methyladenosine methylation landscape of human normal skin and middle ear cholesteatoma

Project description:To determine the lncRNA and mRNA m6A quantity and expression profile in middle ear cholesteatoma and normal skin tissues, we used lncRNA and mRNA epitranscriptome microArray analysis from Arraystar to examine the RNA m6A and expression levels in middle ear cholesteatoma and normal skin tissues.

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Transcription profiling of mouse osteoclastogenic splenocytes

Project description:Effect of c-fos expression in osteoclastogenic splenocytes.

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Bone Marrow Monocyte/Macrophage Derived Activin A Mediates the Osteoclastogenic Effects of IL-3 in Myeloma

Project description:Myeloma bone disease is characterized by tremendous bone destruction with suppressed bone formation. IL-3 is a multifunctional cytokine that increases myeloma cell growth and osteoclast proliferation while inhibiting osteoblast differentiation. While IL-3 appears to be an attractive therapeutic target for myeloma, attempts at targeting IL-3 have been unsuccessful due to IL-3’s effects on normal hematopoiesis. Thus identification of IL-3’s downstream effects in MMBD is important for effective targeting of this cytokine in MM. Here we demonstrated that treatment of myeloma patient CD14+ bone marrow monocyte / macrophages with IL-3 induces high levels of Activin A (ActA), a pluripotent TGF-β superfamily member that, like IL-3, modulates MMBD by enhancing osteoclastogenesis and inhibiting osteoblasts. We show that IL-3 induced osteoclastogenesis is mediated by ActA and is RANKL independent. Additionally, IL-3 induced ActA secretion is greatest early in osteoclastogenesis and ActA acts early in osteoclastogenesis. Therefore we suggest that therapies targeting ActA production should block IL-3’s effects in myeloma bone disease.

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Project description:To investigate the differential expression profiling of circular RNAs (circRNAs) between acquired middle ear cholesteatoma and normal skin, and to identify potential circRNAs contributing to the etiopathogenesis of middle ear cholesteatoma, circRNA microarray analysis and functional prediction were performed.

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