Abstract
BackgroundThe lung is an important target organ for hypoxia treatment, and hypoxia can induce several diseases in the body.MethodsWe performed transcriptome sequencing for the lungs of rats exposed to plateau hypoxia at 0 day and 28 days. Sequencing libraries were constructed, and enrichment analysis of the differentially expressed genes (DEGs) was implemented using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Subsequently, experimental validation was executed by quantitative real-time PCR (qRT-PCR) and western blot.ResultsThe results showed that the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) signaling pathway that was involved in immunity may play a crucial function in lung injury caused by plateau hypoxia. And the expressions of NOD1, NOD2, IL-1β, TNF-α, IL-6, and IL-18 were higher at 28 days of exposure to plateau hypoxia than that at 0 day. Similarly, CARD9, MYD88, p38 MAPK, and NF-κB p65, which are related to the NF-κB and MAPK signaling pathways, also demonstrated increased expression at 28 days exposure to plateau hypoxia than at 0 day.ConclusionsOur study suggested that the NFκBp65 and p38 MAPK signaling pathways may be activated in the lungs of rats during plateau hypoxia. Upregulated expression of NFκBp65 and p38 MAPK can promote the transcription of downstream inflammatory factors, thereby aggravating the occurrence and development of lung tissue remodeling.
Highlights
About 2% of the world’s total population lives in highaltitude areas, and in China alone, areas above 3000 m account for 25% of the country’s land [1]
Characterization of the transcriptome sequence To explore the molecular mechanism of lung damage after exposure to plateau hypoxia, three replicates of the samples at 0 day or 28 days were sequenced, and the transcriptome libraries were constructed
The results suggested that the expression levels of the examined genes, including NOD1, NOD2, IL-1β, TNF-α, IL-6, and IL-18, were all increased after exposure to plateau hypoxia
Summary
About 2% of the world’s total population lives in highaltitude areas (generally ≥ 2500 m), and in China alone, areas above 3000 m account for 25% of the country’s land [1]. The majority of NLRs comprise a variable N-terminal effector domain, a central NOD, and a Cterminal leucine-rich repeat (LRR) domain [8]. The earliest discovered NLRs [12, 13], NOD1, and NOD2 are both expressed in the lungs [14,15,16,17,18,19,20]. After NOD1 and NOD2 recognize the PAMPs, the nuclear factor (NF)-κB and MAP kinase (MAPK) signaling pathways are activated through Rip kinase. Severe inflammatory responses are found in HAPE patients [21]. We speculate that the NOD-like receptor signaling pathway may be tightly involved with the occurrence and development of HAPE. The lung is an important target organ for hypoxia treatment, and hypoxia can induce several diseases in the body
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