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pmid:37359021

Bioinformatic analysis of the molecular mechanisms underlying the progression of bone defects.

Hao Liu · Xuan Zhao · Yin Li · Jiang Yi · Chenxi Zhang · Ziyang Zheng · Siming Dai · Guoyong Yin · Shujie Zhao

Frontiers in medicine · 2023 doi:10.3389/fmed.2023.1157099

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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title
Bioinformatic analysis of the molecular mechanisms underlying the progression of bone defects.
doi
10.3389/fmed.2023.1157099
pmid
37359021
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Hao Liu
[1]
Xuan Zhao
[2]
Yin Li
[3]
Jiang Yi
[4]
Chenxi Zhang
[5]
Ziyang Zheng
[6]
Siming Dai
[7]
Guoyong Yin
[8]
Shujie Zhao
journal
Frontiers in medicine
year
2023
abstract
Background: The pathophysiology of bone defects (BDs) is complex, and the treatment for bone defects, in particular massive bone defects, remains a major clinical challenge. Our study was conducted to explore the molecular events related to the progression of bone defects a common clinical condition. Methods: First, microarray data of GSE20980 were obtained from the Gene Expression Omnibus (GEO) database, where 33 samples in total were used to analyze the molecular biological processes related to bone defects. Next, the original data were normalized and differentially expressed genes (DEGs) were identified. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. Finally, a protein-protein interaction (PPI) network was constructed and the trends of the different genes were confirmed. Results: Compared with the samples of non-critical size defects (NCSD), the samples of critical size defects (CSD) had 2057, 827, and 1,024 DEGs at 7, 14, and 21 days post injury, respectively. At day 7, the DEGs were significantly enriched in metabolic pathways, at day 14 the DEGs were predominantly enriched in G-protein coupled signaling pathways and the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway, and at day 21 the DEGs were mainly enriched in circadian entrainment and synaptic-related functions. The PPI network showed similar results. Quantitative real-time PCR (qRT-PCR) and western blot (WB) were performed to validate the partial results of sequencing. Conclusion: This study provides some clues about the molecular mechanism behind bone defects, which should contribute to scientific research and clinical treatment of this condition.
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The Student’s t-test was used to identify DEGs with an average fold-change of >2.0, and p < 0.05 was considered to indicate a statistically significant difference.
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Compared with NCSD samples, CSD samples had 2,057, 827, and 1,024 differentially expressed genes at 7, 14, and 21 days post injury, respectively.
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Compared with the samples of non-critical size defects (NCSD), the samples of critical size defects (CSD) had 2057, 827, and 1,024 DEGs at 7, 14, and 21 days post injury, respectively.
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Temporal Gene Expression Profiling of Bone Repair in a Rat Calvarial Defect
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a common clinical condition. Methods: First, microarray data of GSE20980 were obtained from the Gene
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Our study was conducted to explore the molecular events related to the progression of bone defects a common clinical condition.\nMethods: First, microarray data of GSE20980 were obtained from the Gene Expression Omnibus (GEO) database, where 33 samples in total were used to analyze the molecular biological processes related to bone defects. Next, the original data were normalized and differentially expressed genes (DEGs) were identified. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. Finally, a protein-protein interaction (PPI) network was constructed and the trends of the different genes were confirmed.\nResults: Compared with the samples of non-critical size defects (NCSD), the samples of critical size defects (CSD) had 2057, 827, and 1,024 DEGs at 7, 14, and 21 days post injury, respectively. 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