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      Sequencing the exons of human glucocorticoid receptor ( NR3C1) gene in Han Chinese with high-altitude pulmonary edema

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          Abstract

          Background

          High-altitude pulmonary edema (HAPE) is a serious acute mountain sickness that mainly occurs in non-acclimatized individuals after rapid ascent to high altitude. The precise etiology of HAPE remains unclear. This study aimed to investigate whether NR3C1 gene polymorphism is associated with the susceptibility to HAPE.

          Methods

          The exons of NR3C1 gene were sequenced by a ABI 3730 DNA analyzer in 133 HAPE patients and matched 135 healthy Han Chinese controls from the Yushu area in Qinghai (the altitude greater than 3500 m).

          Results

          DNA sequencing showed the heterozygous substitutions at codon 588 (rs6194) in exon 6 and 766 (rs6196) in exon 9 of NR3C1 gene. The genotypic distributions and allelic frequencies of NR3C1 SNP rs6194 showed significant differences in two groups ( P < 0.05). The frequencies of the C allele were significantly higher in the HAPE group than in the control group ( P < 0.05) with an odds ratio of 3.009 (95% CI = 1.250-7.244). There were no differences in genotypic and allelic frequencies in rs6196 polymorphism between the two groups.

          Conclusions

          NR3C1 gene rs6194 polymorphism is correlated with HAPE susceptibility. CC genotype and C allele of rs6194 polymorphism might increase the risk of HAPE in Han Chinese.

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          Most cited references16

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          High-altitude illness.

          P Hackett, R C Roach (2001)
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            Crucial Role for Ecto-5′-Nucleotidase (CD73) in Vascular Leakage during Hypoxia

            Linda F. Thompson, Holger Eltzschig, Juan Ibla … (2004)
            Extracellular adenosine has been widely implicated in adaptive responses to hypoxia. The generation of extracellular adenosine involves phosphohydrolysis of adenine nucleotide intermediates, and is regulated by the terminal enzymatic step catalyzed by ecto-5′-nucleotidase (CD73). Guided by previous work indicating that hypoxia-induced vascular leakage is, at least in part, controlled by adenosine, we generated mice with a targeted disruption of the third coding exon of Cd73 to test the hypothesis that CD73-generated extracellular adenosine functions in an innate protective pathway for hypoxia-induced vascular leakage. Cd73 −/− mice bred and gained weight normally, and appeared to have an intact immune system. However, vascular leakage was significantly increased in multiple organs, and after subjection to normobaric hypoxia (8% O2), Cd73 −/− mice manifested fulminant vascular leakage, particularly prevalent in the lung. Histological examination of lungs from hypoxic Cd73 −/− mice revealed perivascular interstitial edema associated with inflammatory infiltrates surrounding larger pulmonary vessels. Vascular leakage secondary to hypoxia was reversed in part by adenosine receptor agonists or reconstitution with soluble 5′-nucleotidase. Together, our studies identify CD73 as a critical mediator of vascular leakage in vivo.
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              High altitude increases circulating interleukin-6, interleukin-1 receptor antagonist and C-reactive protein.

              M. H. Tschöp, M Toepfer, H Hautmann … (2000)
              Hypoxic pulmonary vasoconstriction is associated with but may not be sufficient for the development of high-altitude pulmonary oedema (HAPO). Hypoxia is known to induce an inflammatory response in immune cells and endothelial cells. It has been speculated that hypoxia-induced inflammatory cytokines at high altitude may contribute to the development of HAPO by causing capillary leakage in the lung. We were interested if such an inflammatory response, possibly involved in a later development of HAPO, is detectable at high altitude in individuals without HAPO. We examined the plasma levels of interleukin 6 (IL-6), interleukin 1 receptor antagonist (IL-1ra) and C-reactive protein (CRP) in two independent studies: study A, Jungfraujoch, Switzerland, three overnight stays at 3458 m, n=12; study B: Capanna Regina Margherita, Italy, 3 overnight stays at 3647 m and one overnight stay at 4559 m, n=10. In both studies, probands showed symptoms of acute mountain sickness but no signs of HAPO. At the Jungfraujoch, IL-6 increased from 0.1+/-0.03 pg/ml to 2. 0+/-0.5 pg/ml (day 2, P=0.03), IL-1ra from 101+/-21 to 284+/-73 pg/ml (day 2, P=0.01), and CRP from 1.0+/-0.4 to 5.8+/-1.5 micrograms/ml (day 4, P=0.01). At the Capanna Margherita, IL-6 increased from 0. 5+/-0.2 pg/ml to 2.0+/-0.8 pg/ml (P=0.02), IL-1ra from 118+/-25 to 213+/-28 pg/ml (P=0.02), and CRP from 0.4+/-0.03 to 3.5+/-1.1 micrograms/ml (P=0.03). IL-8 was below the detection limit of the ELISA (<25 pg/ml) in both studies. The increase of IL-6 and IL-1ra in response to high altitude was delayed and preceded the increase of CRP. We conclude that: (1) circulating IL-6, IL-1ra and CRP are upregulated in response to hypobaric hypoxic conditions at high altitude, and (2) the moderate systemic increase of these inflammatory markers may reflect considerable local inflammation. The existence and the kinetics of high altitude-induced cytokines found in this study support the hypothesis that inflammation is involved in the development of HAPO. Copyright 2000 Academic Press.
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                Author and article information

                Contributors
                Hui Du: 875747811@qq.com
                Jing Zhao: 624302514@qq.com
                Zhanhai Su: 1817901@qq.com
                Yongnian Liu: liuyongnian@qhu.edu.cn
                Yingzhong Yang: +86-971-8175660 , yingzhong-yang@hotmail.com
                Journal
                Journal ID (nlm-ta): J Physiol Anthropol
                Journal ID (iso-abbrev): J Physiol Anthropol
                Title: Journal of Physiological Anthropology
                Publisher: BioMed Central (London )
                ISSN (Print): 1880-6791
                ISSN (Electronic): 1880-6805
                Publication date (Electronic): 27 March 2018
                Publication date PMC-release: 27 March 2018
                Publication date Collection: 2018
                Volume: 37
                Electronic Location Identifier: 7
                Affiliations
                [1 ]GRID grid.262246.6, Department of Basic Medical Sciences, Medical College, , Qinghai University, ; Xining, 810001 Qinghai China
                [2 ]GRID grid.262246.6, Research Center for High Altitude Medical Sciences, Medical College, , Qinghai University, ; Xining, 810001 Qinghai China
                Article
                Publisher ID: 168
                DOI: 10.1186/s40101-018-0168-8
                PMC ID: 5869773
                SO-VID: c1143963-e166-493a-8eba-8f46cab8c0f2
                Copyright © © The Author(s). 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 24 January 2018
                Date accepted : 13 March 2018
                Funding
                Funded by: Basic Applied Study Foundation of Qinghai
                Award ID: 2016-ZJ-706
                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Anthropology
                Keywords: nr3c1,exon,snp,hape,susceptibility
                Data availability:
                ScienceOpen disciplines: Anthropology
                Keywords: nr3c1, exon, snp, hape, susceptibility

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