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Published on: January 7, 2019
mRNA expression profiling and pathway analysis of chronic intermittent hypoxia-induced pancreatic injury in ob/ob
Yaopeng Guo1, Shengquan Huang2, Jiayi Lin1
1Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Background:
Increasing evidence suggests that messenger RNA (mRNA) is centrally involved in the initiation and progression of various diseases. However, its involvement in pancreatic injury resulting from obstructive sleep apnea (OSA) continues to be incompletely elucidated. The present investigation aimed to characterize mRNA expression changes using a murine model of chronic intermittent hypoxia (CIH) to provide new insights into the mechanisms underlying OSA-associated pancreatic injury.
Methods:
An ob/ob murine model for pancreatic injury triggered by CIH was established. RNA sequencing (RNA-seq) was conducted to detect differentially expressed mRNAs, and subsequently Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were applied to delineate the associated functional annotations and signaling cascades. Furthermore, several selected mRNAs were validated using reverse transcription PCR (RT-qPCR). Finally, we constructed a protein-protein interaction (PPI) network to delineate the interplay among the protein targets of the differentially expressed genes (DEGs).
Results:
In a mouse model of CIH-induced pancreatic dysfunction, 481 mRNAs were upregulated and 165 were downregulated. KEGG enrichment analysis indicated that the NOD-like receptor signaling pathway is implicated in CIH-induced pancreatic dysfunction. Subsequently, several differentially expressed mRNAs were subjected to RT-qPCR validation. On the basis of these data, a subset of DEGs were selected to construct a PPI network.
Conclusion:
Overall, we identified 646 DEGs in the CIH mouse model. These results may offer important perspectives on the pathophysiological processes that underlie OSA-induced diabetes mellitus.
Insights
Messenger RNA (mRNA) changes in obstructive sleep apnea (OSA) linked to pancreatic injury were identified. Chronic intermittent hypoxia (CIH) in mice revealed 646 differentially expressed genes (DEGs), implicating the NOD-like receptor pathway.
Area of Science:
- Molecular Biology
- Pathophysiology
- Genomics
Background:
- Messenger RNA (mRNA) plays a role in various diseases.
- The specific role of mRNA in pancreatic injury due to obstructive sleep apnea (OSA) is not fully understood.
- This study investigates mRNA expression changes in a mouse model of chronic intermittent hypoxia (CIH) to understand OSA-associated pancreatic injury.
Purpose of the Study:
- To characterize mRNA expression alterations in pancreatic tissue under chronic intermittent hypoxia (CIH) conditions.
- To identify key molecular pathways involved in OSA-related pancreatic dysfunction.
- To provide insights into the mechanisms of pancreatic injury in the context of OSA.
Main Methods:
- Utilized an ob/ob mouse model subjected to CIH to induce pancreatic injury.
- Employed RNA sequencing (RNA-seq) to identify differentially expressed mRNAs (DEGs).
- Performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
- Validated selected DEGs using reverse transcription PCR (RT-qPCR) and constructed a protein-protein interaction (PPI) network.
Main Results:
- Identified a total of 646 DEGs in the CIH mouse model, with 481 mRNAs upregulated and 165 downregulated.
- KEGG pathway analysis highlighted the NOD-like receptor signaling pathway as significantly implicated in CIH-induced pancreatic dysfunction.
- Validated key DEGs and constructed a PPI network to illustrate molecular interactions.
Conclusions:
- The study identified significant mRNA expression changes in the pancreas due to CIH, relevant to OSA.
- The findings suggest the NOD-like receptor signaling pathway is a key player in OSA-associated pancreatic injury.
- These results offer perspectives on the pathophysiology of OSA-induced diabetes mellitus.
