No Correlation between Plasma Levels of Vascular Endothelial Growth Factor or its Soluble Receptor and Acute Mountain Sickness

Schommer, Kai; Wiesegart, Neele; Dehnert, Christoph; Mairbäurl, Heimo; Bärtsch, Peter

doi:10.1089/ham.2011.1020

Cited by 14 publications

(16 citation statements)

References 24 publications

(32 reference statements)

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“…, Schommer et al . ). Alternatively, the soluble VEGF receptor (SFlt1) may bind circulating VEGF and reduce free plasma VEGF and therefore VEGF activity (Chen et al .…”

Section: Potential Drug Targets For Preventing Amsmentioning

confidence: 97%

“…SNP rs3025039, but not SNP rs3025030, was also significantly associated with plasma VEGF levels. But there is no evidence of a direct association between plasma VEGF levels and AMS (Dorward et al 2007, Schommer et al 2011. Alternatively, the soluble VEGF receptor (SFlt1) may bind circulating VEGF and reduce free plasma VEGF and therefore VEGF activity (Chen et al 2000).…”

Section: Vegfmentioning

confidence: 99%

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In search for better pharmacological prophylaxis for acute mountain sickness: looking in other directions

Wang

Xiong

et al. 2015

Acta Physiologica

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Despite decades of research, the exact pathogenic mechanisms underlying acute mountain sickness (AMS) are still poorly understood. This fact frustrates the search for novel pharmacological prophylaxis for AMS. The prevailing view is that AMS results from an insufficient physiological response to hypoxia and that prophylaxis should aim at stimulating the response. Starting off from the opposite hypothesis that AMS may be caused by an initial excessive response to hypoxia, we suggest that directly or indirectly blunting-specific parts of the response might provide promising research alternatives. This reasoning is based on the observations that (i) humans, once acclimatized, can climb Mt Everest experiencing arterial partial oxygen pressures (PaO2) as low as 25 mmHg without AMS symptoms; (ii) paradoxically, AMS usually develops at much higher PaO2 levels; and (iii) several biomarkers, suggesting initial activation of specific pathways at such PaO2, are correlated with AMS. Apart from looking for substances that stimulate certain hypoxia triggered effects, such as the ventilatory response to hypoxia, we suggest to also investigate pharmacological means aiming at blunting certain other specific hypoxia-activated pathways, or stimulating their agonists, in the quest for better pharmacological prophylaxis for AMS.

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“…, Schommer et al . ). Alternatively, the soluble VEGF receptor (SFlt1) may bind circulating VEGF and reduce free plasma VEGF and therefore VEGF activity (Chen et al .…”

Section: Potential Drug Targets For Preventing Amsmentioning

confidence: 97%

Section: Vegfmentioning

confidence: 99%

In search for better pharmacological prophylaxis for acute mountain sickness: looking in other directions

Wang

Xiong

et al. 2015

Acta Physiologica

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“…Evidence regarding VEGF from AMS studies remains controversial. Absolute values or changes in VEGF were not correlated with AMS scores [ 46 , 47 ]. On the other hand, Ding et al reported that among Chinese Han subjects ( n = 40), the AMS group had a higher VEGF plasma concentration than the control group at both sea level and HA [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

EPAS1 and VEGFA gene variants are related to the symptoms of acute mountain sickness in Chinese Han population: a cross-sectional study

et al. 2020

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Background More people ascend to high altitude (HA) for various activities, and some individuals are susceptible to HA illness after rapidly ascending from plains. Acute mountain sickness (AMS) is a general complaint that affects activities of daily living at HA. Although genomic association analyses suggest that single nucleotide polymorphisms (SNPs) are involved in the genesis of AMS, no major gene variants associated with AMS-related symptoms have been identified. Methods In this cross-sectional study, 604 young, healthy Chinese Han men were recruited in June and July of 2012 in Chengdu, and rapidly taken to above 3700 m by plane. Basic demographic parameters were collected at sea level, and heart rate, pulse oxygen saturation (SpO 2 ), systolic and diastolic blood pressure and AMS-related symptoms were determined within 18–24 h after arriving in Lhasa. AMS patients were identified according to the latest Lake Louise scoring system (LLSS). Potential associations between variant genotypes and AMS/AMS-related symptoms were identified by logistic regression after adjusting for potential confounders (age, body mass index and smoking status). Results In total, 320 subjects (53.0%) were diagnosed with AMS, with no cases of high-altitude pulmonary edema or high-altitude cerebral edema. SpO 2 was significantly lower in the AMS group than that in the non-AMS group ( P = 0.003). Four SNPs in hypoxia-inducible factor-related genes were found to be associated with AMS before multiple hypothesis testing correction. The rs6756667 ( EPAS1 ) was associated with mild gastrointestinal symptoms ( P = 0.013), while rs3025039 ( VEGFA ) was related to mild headache ( P = 0.0007). The combination of rs6756667 GG and rs3025039 CT/TT further increased the risk of developing AMS ( OR = 2.70, P < 0.001). Conclusions Under the latest LLSS, we find that EPAS1 and VEGFA gene variants are related to AMS susceptibility through different AMS-related symptoms in the Chinese Han population; this tool might be useful for screening susceptible populations and predicting clinical symptoms leading to AMS before an individual reaches HA. Trial registration Chinese Clinical Trial Registration, ChiCTR-RCS-12002232 . Registered 31 May 2012.

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“…Strenuous physical work at high altitudes is accompanied by higher levels of VEGF and pulmonary artery pressure than exercise at sea level (36). Nonetheless, the absolute values of or changes in VEGF expression have not been shown to be correlated with AMS symptoms or scores (37). Hypoxia leads to increased hydrostatic pressure and blood‐brain barrier permeability in patients with acute ischemic stroke through VEGF (38).…”

Section: Discussionmentioning

confidence: 99%

Roles of the hypoximir microRNA‐424/322 in acute hypoxia and hypoxia‐induced pulmonary vascular leakage

Tsai

Huang

Tsai³

et al. 2019

The FASEB Journal

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Acute mountain sickness (AMS) occurs in up to 25% of unacclimatized persons who ascend to 3000 m and can result in high‐altitude pulmonary edema (HAPE). MicroRNAs (miRs) can regulate gene expression at the post‐transcriptional level. Hypoxia selectively disrupts endothelial tight junction complexes through a hypoxia‐inducible factor‐1α (HIF‐1α)‐dependent mechanism. Though increased HIF‐1α expression is associated with adaptation and protection from AMS development in the early stage of hypoxia, a downstream effector of HIF‐1a, VEGF, can induce overzealous endothelial barrier dysfunction, increase vascular permeability, and ultimately result in HAPE and high‐altitude cerebral edema. We hypothesized that the fine‐tuning of downstream effectors by miRs is paramount for the preservation of endothelial barrier integrity and the prevention of vascular leakage. We found that several miRs were up‐regulated in healthy volunteers who were subjected to a 3100‐m height. By reviewing the literature and using online bioinformatics prediction software, we specifically selected miR‐424 for further investigation because it can modulate both HIF‐1α and VEGF. Hypoxia‐induced miR‐424 overexpression is HIF‐1α dependent, and miR‐424 stabilized HIF‐1α, decreased VEGF expression, and promoted vascular endothelial cadherin phosphorylation. In addition, hypoxia resulted in endothelial barrier dysfunction with increased permeability; miR‐424 thus attenuated hypoxia‐induced endothelial cell senescence and apoptosis. miR‐322 knockout mice were susceptible to hypoxia‐induced pulmonary vascular leakage. miR‐322 mimics improved hypoxia‐induced pulmonary vascular leakage in vivo. We conclude that several miRs were up‐regulated in healthy adult volunteers subjected to hypobaric hypoxemia. miR‐424/322 could modulate the HIF‐1α‐VEGF axis and prevent hypoxia‐induced pulmonary vascular leakage under hypoxic conditions.—Tsai, S.‐H., Huang P.‐H., Tsai, H.‐Y., Hsu, Y.‐J., Chen, Y.‐W., Wang, J.‐C., Chen, Y.‐H., Lin, S.‐J. Roles of the hypoximir microRNA‐424/322 in acute hypoxia and hypoxia‐induced pulmonary vascular leakage. FASEB J. 33, 12565–12575 (2019). http://www.fasebj.org

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No Correlation between Plasma Levels of Vascular Endothelial Growth Factor or its Soluble Receptor and Acute Mountain Sickness

Cited by 14 publications

References 24 publications

In search for better pharmacological prophylaxis for acute mountain sickness: looking in other directions

In search for better pharmacological prophylaxis for acute mountain sickness: looking in other directions

EPAS1 and VEGFA gene variants are related to the symptoms of acute mountain sickness in Chinese Han population: a cross-sectional study

Roles of the hypoximir microRNA‐424/322 in acute hypoxia and hypoxia‐induced pulmonary vascular leakage

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