Maternal Adaptation to High-altitude Pregnancy: An Experiment of Nature—A Review

Moore, Lorna G.; Shriver, Mark D.; Bemis, Lynne T.; Hickler, B.; Wilson, Megan J.; Brutsaert, Tom D.; Parra, Esteban J.; Vargas, Enrique

doi:10.1016/j.placenta.2004.01.008

Cited by 187 publications

(172 citation statements)

References 115 publications

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“…In humans, the potential fitness consequences of excessive polycythemia seem especially clear cut when considering the effects on pregnancy outcomes at high altitude (Moore et al, 2004;Gonzales et al, 2009;Julian et al, 2009a;Julian et al, 2009b). Hospital-based studies have documented that the risk of adverse perinatal outcomes is increased with extreme maternal Hcts (Moore et al, 2001a;Gonzales et al, 2009) (Fig.4).…”

Section: Erythropoeitic Activitymentioning

confidence: 99%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

346

343

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SummaryHigh-altitude environments provide ideal testing grounds for investigations of mechanism and process in physiological adaptation. In vertebrates, much of our understanding of the acclimatization response to high-altitude hypoxia derives from studies of animal species that are native to lowland environments. Such studies can indicate whether phenotypic plasticity will generally facilitate or impede adaptation to high altitude. Here, we review general mechanisms of physiological acclimatization and genetic adaptation to high-altitude hypoxia in birds and mammals. We evaluate whether the acclimatization response to environmental hypoxia can be regarded generally as a mechanism of adaptive phenotypic plasticity, or whether it might sometimes represent a misdirected response that acts as a hindrance to genetic adaptation. In cases in which the acclimatization response to hypoxia is maladaptive, selection will favor an attenuation of the induced phenotypic change. This can result in a form of cryptic adaptive evolution in which phenotypic similarity between high-and low-altitude populations is attributable to directional selection on genetically based trait variation that offsets environmentally induced changes. The blunted erythropoietic and pulmonary vasoconstriction responses to hypoxia in Tibetan humans and numerous high-altitude birds and mammals provide possible examples of this phenomenon. When lowland animals colonize high-altitude environments, adaptive phenotypic plasticity can mitigate the costs of selection, thereby enhancing prospects for population establishment and persistence. By contrast, maladaptive plasticity has the opposite effect. Thus, insights into the acclimatization response of lowland animals to high-altitude hypoxia can provide a basis for predicting how altitudinal range limits might shift in response to climate change.

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Section: Erythropoeitic Activitymentioning

confidence: 99%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

346

343

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“…Nevertheless, native Andean highland populations are characterized by a lower perinatal mortality and higher birth weight than nonindigenous lowland populations living at high altitude (Gonzales, 2007). In addition to a better uteroplacental oxygen supply in the indigenous highland population (Moore et al, 1986(Moore et al, , 2004, there might be genetic adaptations resulting in a better oxygen supply to the fetus. Since oxygen is reversibly bound to hemoglobin, hemoglobin genes are possible candidates for genetic adaptation to high altitude.…”

Section: Introductionmentioning

confidence: 99%

Native highland and lowland populations differ in .GAMMA.-globin gene promoter polymorphisms related to altered fetal hemoglobin levels and delayed fetal to adult globin switch after birth

Rottgardt

Rothhammer

Dittmar

2010

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Lowered partial oxygen pressure at high altitude exerts a strong selection pressure. Since hypoxia is most serious for the fetus, fetal hemoglobin genes (HBG1, HBG2) are candidates for genetic adaptation to high altitude. The aim of this study was to compare promoter polymorphisms of these genes for differences between highland and lowland populations. In 50 native highlanders of the Chilean Andes and 50 lowlanders of European ancestry, the promoters of HBG1 and HBG2 genes were sequenced. In the HBG1 promoter, the 4-basepair AGCA deletion was less frequently present in highlanders than in lowlanders (10% vs. 24%, P = 0.014). In the HBG2 promoter, the frequency of the T allele of the common −158 C > T polymorphism was decreased in highlanders, compared with lowlanders (8% vs. 34%, P = 0.000009). A combined analysis of both markers showed that none of the highlanders with the AGCA deletion carried the HBG2 T allele, in contrast to 43% of lowlanders (P = 0.030). Since the AGCA deletion is associated with diminished expression of fetal γ globin chains, it might affect fetal oxygen supply at high altitude. Both the AGCA deletion and the HBG2 −158 T allele are associated with a delayed fetal to adult globin switch after birth, resulting in a delayed production of adult hemoglobin, thereby possibly affecting the oxygen supply of infants at high altitude.

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“…There are still limited and somewhat controversial data about genetic polymorphisms and related susceptibility to HAI. For example, endothelial nitric oxide synthase gene polymorphisms were associated with susceptibility to high-altitude pulmonary edema in Japan (Droma et al 2002) but not in Europe (Weiss et al 2003); singlenucleotide polymorphisms (SNPs) of the endothelin-1 (the potent hypoxia-inducible factor [HIF]-targeted vasoconstrictor) gene also differ in the Andeans compared with low-altitude populations (Moore et al 2004). Various biochemical mediators such as nitric oxide (NO), endothelin-1, and the renin-angiotensin-aldosterone system and possible oxygen-sensing mechanisms may be involved in hypoxic adaptation such as HIF-1, and individuals who have had high-altitude pulmonary edema once run an unpredictable but significant risk of recurrence; therefore, there are constitutional or genetic components in the etiology of HAI (Woods and Montgomery 2001;Mortimer et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Association of hsp70-2 and hsp-hom gene polymorphisms with risk of acute high-altitude illness in a Chinese population

Fang

Wang

Li³

et al. 2005

Cell Stress Chaper

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High-altitude illness (HAI) is a potentially fatal condition involving genetic and environmental components. Accumulated experimental evidence suggests that heat shock proteins (Hsps), especially HSP70, can protect cells and organs against different types of damage. We investigated whether genetic variation in constitutive and inducible hsp70 genes could be associated with risk of HAI. The association between polymorphisms of the HSP70 family genes and risk of HAI was determined in 56 patients with HAI and in 100 matched controls by genotyping for the polymorphisms ϩ190 G/C, ϩ1267 A/G, 2437 G/C in the hsp70-1, hsp70-2, and hsp70-hom genes by using polymerase chain reaction-restriction fragment length polymorphism. The data showed that there was no statistically significant difference in the genotype and allele distributions of hsp70-1, in hsp70-2 allele and hsp70-2 A/A and A/B genotypes, and in allele distribution of hsp70-hom among patients with HAI and controls ( 2 test, P Ͼ 0.05). However, there was a significantly higher frequency of hsp70-2 B/B and hsp70-hom A/A and B/B genotypes and a significantly lower frequency of the hsp70-hom A/B genotype in the HAI patients compared with the controls (P Ͻ 0.05 for all). The risk associated with the hsp70-2 B/B and hsp70-hom A/A, A/B, and B/B genotypes were 4.017 (95% CI ϭ 1.496-10.781; P ϭ 0.004), 2.434 (95% CI ϭ 1.184-5.003; P ϭ 0.012), 0.299 (95% CI ϭ 0.148-0.602, P ϭ 0.001), and 5.880 (95% CI ϭ1. 145-30.196, P ϭ 0.026), respectively. Our results suggest that individuals with hsp70-2 B/B and hsp70-hom A/B and B/B genotypes may be more susceptible to HAI, whereas those with hsp70-hom A/B genotype may be tolerant to HAI. Further studies in individuals of different age and sex are warranted to elucidate the underlying mechanisms of this association and the possible functions of different genotypes of hsp70-2 and hsp70-hom under hypoxic stress.

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Maternal Adaptation to High-altitude Pregnancy: An Experiment of Nature—A Review

Cited by 187 publications

References 115 publications

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Native highland and lowland populations differ in .GAMMA.-globin gene promoter polymorphisms related to altered fetal hemoglobin levels and delayed fetal to adult globin switch after birth

Association of hsp70-2 and hsp-hom gene polymorphisms with risk of acute high-altitude illness in a Chinese population

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