Background: The occurrence of acute mountain sickness (AMS), which develops in some individuals who ascend to altitudes above 2,500 m, may be associated with 4 hypoxia-related genes (HIF-1, VEGFA, HSP-70 and eNOS). Objectives: The aim of our study was to investigate the potential role of the 4 hypoxia-related genes in AMS pathogenesis. We therefore evaluated single-nucleotide polymorphisms (SNPs) of the genes in an association study using a case-control design. Methods: At an altitude of 4,600 m, 64 male Chinese patients with AMS, defined according to the Lake Louise consensus criteria, were compared to 64 Chinese men free of symptoms of AMS. Clinical data, such as age, history of diseases, oxygen saturation (SpO₂) and heart rate, were obtained. Genotypes of selected SNPs of these genes in patients were compared with those in controls. Results: The mean SpO₂ and heart rate of the AMS and control groups were similar before ascent to high altitude (p = 0.79, p = 0.62) but, 24 h after ascent, the mean SpO₂ of the AMS group was significantly lower than that of the control group (p = 0.001), and the mean heart rate of the AMS group was significantly higher than that of the control group (p = 0.001). Twenty-eight of the 48 SNPs investigated were successfully genotyped, and SNP allele frequencies were obtained. The rs3025039 SNP and the haplotype (rs1413711, rs833070 and rs3025000) in the VEGFA gene were significantly associated with AMS (p = 0.0435 and 0.024, respectively). Conclusions: Our study demonstrates a possible association between the VEGFA gene and AMS. We conclude that VEGFA may have an important role in the AMS process.

OBJECTIVE: This study investigated associations between polymorphisms in the vascular endothelial growth factor (VEGF) gene and susceptibility to acute mountain sickness. METHODS: Two hundred Han Chinese soldiers who developed acute mountain sickness after rapidly ascending to an altitude of < 3600 m and 200 control soldiers (who did not develop the condition) were enrolled in the study. Twelve single nucleotide polymorphisms (SNPs) of the VEGF gene were genotyped in all the study participants. Plasma VEGF concentrations were measured by enzymelinked immunosorbent assay in 40 subjects with acute mountain sickness and 40 controls before and after exposure to high altitude. RESULTS: The frequencies of the rs3025039 genotype and allele were significantly different between the groups. Two SNPs, rs3025039 (which involves a C→T allele variation at position 936 in the 3′ untranslated region) and rs3025030 (which involves a G→C allele variation in the intronic sequence), were associated with a decreased risk of acute mountain sickness. CONCLUSION: The SNPs rs3025039 and rs3025030 of the VEGF gene may be associated with a decreased risk of acute mountain sickness development.

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Acute lung injury (ALI) induced by bacteria LPS is characterized by the upregulation of the apoptosis rate of tissue cells and aggravation of inflammatory response. Although many studies have focused on the pathogenesis of this disease, its mechanism remains unknown. This study examined the regulatory role of long non-coding RNA (lncRNA) LINC01194 in the progression of ALI through various bioinformatics analyses and experimental work, including ELISA assay, dual-luciferase reporter assay, biotinylated RNA pull-down assay, and western blot analysis. The result showed that the LINC01194 was overexpressed in the ALI-induced mice model. We observed a significant upregulation of LINC01194 in LPS-treated Mouse lung epithelial type II cells (MLE-12 cells) after 24 hrs of induction. Bioinformatics analysis, Elisa assay, qRT-PCR analysis, Biotinylated RNA pull-down assay, apoptosis test, and western blot analysis demonstrated that the LINC01194 could act as a miR-203a-3p sponge to activate the inflammatory response in LPS-induced ALI model through post-transcriptional upregulation of MIP-2. We showed that LINC01194 regulates the inflammatory response and apoptosis of LPS-induced mice and MLE-12 cells via the miR-203a-3p/MIP-2 axis. LINC01194 could be a potential biomarker for early diagnosis and the treatment of ALI.

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