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A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip

OBJECTIVE: To date, exhaustive gene expression analyses of chondrocytes in hip osteoarthritis (OA) have yielded specific gene expression patterns. No study has reported on the exhaustive transcriptome of secondary hip OA based on acetabular dysplasia in a Japanese population, while previous reports...

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Autores principales: Aki, Takashi, Hashimoto, Ko, Ogasawara, Masanori, Itoi, Eiji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019400/
https://www.ncbi.nlm.nih.gov/pubmed/29944724
http://dx.doi.org/10.1371/journal.pone.0199734
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author Aki, Takashi
Hashimoto, Ko
Ogasawara, Masanori
Itoi, Eiji
author_facet Aki, Takashi
Hashimoto, Ko
Ogasawara, Masanori
Itoi, Eiji
author_sort Aki, Takashi
collection PubMed
description OBJECTIVE: To date, exhaustive gene expression analyses of chondrocytes in hip osteoarthritis (OA) have yielded specific gene expression patterns. No study has reported on the exhaustive transcriptome of secondary hip OA based on acetabular dysplasia in a Japanese population, while previous reports have focused on primary or idiopathic hip OA in Caucasian populations. This study aims to search for specific gene expression patterns of secondary hip OA chondrocytes by transcriptome analysis. DESIGN: Human articular cartilage was obtained from femoral heads following hemiarthroplasty for femoral neck fracture (N = 8; non-OA) and total hip arthroplasty for secondary hip OA (N = 12). Total RNA was extracted from the articular cartilage and submitted for microarray analysis. The obtained data were used to perform gene expression analysis, GO enrichment analysis and pathway analysis and were compared with data from primary hip OA in Caucasian populations in the literature. RESULTS: We identified 888 upregulated (fold change: FC ≥ 2) and 732 downregulated (FC ≤ 0.5) genes in hip OA versus non-OA chondrocytes, respectively. Only 10% of upregulated genes were common between the secondary and primary OA. The newly found genes prominently overexpressed in the secondary hip OA chondrocytes were DPT, IGFBP7, and KLF2. Pathway analysis revealed extracellular matrix (ECM)-receptor interaction as an OA-related pathway, which was similar to previous reports in primary hip OA. CONCLUSIONS: This is the first study to report the genome-wide transcriptome of secondary hip OA chondrocytes and demonstrates new potential OA-related genes. Gene expression patterns were different between secondary and primary hip OA, although the results of pathway and functional analysis were similar.
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spelling pubmed-60194002018-07-07 A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip Aki, Takashi Hashimoto, Ko Ogasawara, Masanori Itoi, Eiji PLoS One Research Article OBJECTIVE: To date, exhaustive gene expression analyses of chondrocytes in hip osteoarthritis (OA) have yielded specific gene expression patterns. No study has reported on the exhaustive transcriptome of secondary hip OA based on acetabular dysplasia in a Japanese population, while previous reports have focused on primary or idiopathic hip OA in Caucasian populations. This study aims to search for specific gene expression patterns of secondary hip OA chondrocytes by transcriptome analysis. DESIGN: Human articular cartilage was obtained from femoral heads following hemiarthroplasty for femoral neck fracture (N = 8; non-OA) and total hip arthroplasty for secondary hip OA (N = 12). Total RNA was extracted from the articular cartilage and submitted for microarray analysis. The obtained data were used to perform gene expression analysis, GO enrichment analysis and pathway analysis and were compared with data from primary hip OA in Caucasian populations in the literature. RESULTS: We identified 888 upregulated (fold change: FC ≥ 2) and 732 downregulated (FC ≤ 0.5) genes in hip OA versus non-OA chondrocytes, respectively. Only 10% of upregulated genes were common between the secondary and primary OA. The newly found genes prominently overexpressed in the secondary hip OA chondrocytes were DPT, IGFBP7, and KLF2. Pathway analysis revealed extracellular matrix (ECM)-receptor interaction as an OA-related pathway, which was similar to previous reports in primary hip OA. CONCLUSIONS: This is the first study to report the genome-wide transcriptome of secondary hip OA chondrocytes and demonstrates new potential OA-related genes. Gene expression patterns were different between secondary and primary hip OA, although the results of pathway and functional analysis were similar. Public Library of Science 2018-06-26 /pmc/articles/PMC6019400/ /pubmed/29944724 http://dx.doi.org/10.1371/journal.pone.0199734 Text en © 2018 Aki et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Aki, Takashi
Hashimoto, Ko
Ogasawara, Masanori
Itoi, Eiji
A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title_full A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title_fullStr A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title_full_unstemmed A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title_short A whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
title_sort whole-genome transcriptome analysis of articular chondrocytes in secondary osteoarthritis of the hip
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019400/
https://www.ncbi.nlm.nih.gov/pubmed/29944724
http://dx.doi.org/10.1371/journal.pone.0199734
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