Interference with neural crest migration by maternal hyperthermia as a cause of embryonic death due to heart failure

Upfold, J. B.; Smith, Murray; Edwards, M. J.

doi:10.1016/0306-9877(91)90240-y

Cited by 7 publications

(5 citation statements)

References 9 publications

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“…Maternal hyperthermia has been demonstrated to be teratogenic in every animal species studied so far. A minimum rise in core temperature of 2.5°C can produce a number of developmental defects (Upfold et al, 1991). Hyperthermia‐induced defects are usually encountered in the CNS and include an open neural tube, micrencephaly, microphthalmia, and neurogenic contractures.…”

Section: Discussionmentioning

confidence: 99%

“…The incidence and type of defect depends on the species and strain, the stage of development, and the severity of hyperthermic exposure (Edwards, 1968; Arora et al, 1979; Germain et al, 1985; Webster et al, 1985). Cardiovascular malformation combined with skeletal and CNS abnormalities has been reported in embryos of chicken, rat, guinea pig, and monkey (De La Cruz et al, 1966; Hendrickx et al, 1979; Nilsen, 1984; Upfold et al, 1991; Morishima et al, 1995; Buckiova et al, 1998). In a previous study (Aoyama and Yamashina, 1994) we demonstrated that hyperthermic treatment of maternal rats at day 9 of pregnancy induced various severe external malformations in embryos.…”

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confidence: 99%

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Conduction system abnormalities in rat embryos induced by maternal hyperthermia

et al. 2002

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Maternal hyperthermia induces severe malformations in the central nervous system (CNS) in both humans and laboratory animals. These phenomena are accompanied by apoptotic cell death, especially in the developing CNS. Cardiovascular malformations in conjunction with skeletal and CNS abnormalities have been reported in embryos of laboratory animals. In rats, hyperthermic treatment at 43°C for 15 min at day 9 of pregnancy induced various severe external malformations in embryos, such as exencephaly, spina bifida, microphthalmia, anophthalmia, facial cleft or defect, generalized edema, and cardiovascular abnormalities. Examination of the embryonic heart revealed abnormal formation of the conduction system. Although hyperthermia causes marked hemodynamic defects, we could not obtain direct proof of a link between hemodynamic alteration by hyperthermia and malformations of the conduction system. Anat Rec 267: 213-219, 2002.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Conduction system abnormalities in rat embryos induced by maternal hyperthermia

et al. 2002

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“…No embryo with a NTD has so far been successfully carried to term. This implicates problems other than basic CNS damage, and our studies have suggested interference with neural crest migration leads to abnormal development of structures dependent on neural crest with heart failure being a possible cause of embryonic death (Upfold, Smith & Edwards, 1991).…”

Section: Introductionmentioning

confidence: 86%

The induction of neural tube defects by maternal hyperthermia: a comparison of the guinea‐pig and human

Smith

Upfold

Edwards

et al. 1992

Neuropathology Appl Neurobio

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In our recent studies on the effects of maternal hyperthermia on the embryonic guinea-pig, we have demonstrated two 'teratogenic windows' at embryonic days 13 and 21 (E13 and E21). E13 encompasses the period of the closure of the neural groove and anterior neuropore, and E21 the commencement of the cortical plate. The approximate equivalent developmental times in the human are E23-E25 and E49-E56 respectively. In the guinea-pig, maternal hyperthermia at E13 results in a high incidence of neural tube defects (NTD), many open, and associated with other defects such as microphthalmia, and scoliosis or kyphosis. The NTD were most common in the developing hindbrain and all demonstrated considerable infoldings of neural tissue, rosettes of neuroepithelial cells, outpocketings of neural tissue and large cystic cavities beneath the defect. In human examples from the Kyoto Human Embryo Collection, 16 had verified hyperthermic insults at E23-E25 and all had NTD which showed similar deformities to the guinea-pig. Most embryos with such gross defects are aborted in the early fetal period in both species.

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“…Some studies in guinea‐pig, mouse, rat, chick, and zebrafish, have suggested that NC is affected during this condition (Aoyama et al, ; Krausova & Peterka, ; Upfold, Smith, & Edwards, ). A “teratogenic window” at equivalent human embryo stage E10‐E11 (23–25 days), encompasses the period of the closure of the neural groove and anterior neuropore (Smith, Upfold, Edwards, Shiota, & Cawdell‐Smith, ).…”

Section: Physical Agentsmentioning

confidence: 99%

The role of teratogens in neural crest development

Cerrizuela

Vega-Lopez

Aybar

2020

Birth Defects Research

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The neural crest (NC), discovered by Wilhelm His 150 years ago, gives rise to a multipotent migratory embryonic cell population that generates a remarkably diverse and important array of cell types during the development of the vertebrate embryo. These cells originate in the neural plate border (NPB), which is the ectoderm between the neural plate and the epidermis. They give rise to the neurons and glia of the peripheral nervous system, melanocytes, chondrocytes, smooth muscle cells, odontoblasts and neuroendocrine cells, among others. Neurocristopathies are a class of congenital diseases resulting from the abnormal induction, specification, migration, differentiation or death of NC cells (NCCs) during embryonic development and have an important medical and societal impact. In general, congenital defects affect an appreciable percentage of newborns worldwide. Some of these defects are caused by teratogens, which are agents that negatively impact the formation of tissues and organs during development. In this review, we will discuss the teratogens linked to the development of many birth defects, with a strong focus on those that specifically affect the development of the NC, thereby producing neurocristopathies.Although increasing attention is being paid to the effect of teratogens on embryonic development in general, there is a strong need to critically evaluate the specific role of these agents in NC development. Therefore, increased understanding of the role of these factors in NC development will contribute to the planning of strategies aimed at the prevention and treatment of human neurocristopathies, whose etiology was previously not considered.

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Interference with neural crest migration by maternal hyperthermia as a cause of embryonic death due to heart failure

Cited by 7 publications

References 9 publications

Conduction system abnormalities in rat embryos induced by maternal hyperthermia

Conduction system abnormalities in rat embryos induced by maternal hyperthermia

The induction of neural tube defects by maternal hyperthermia: a comparison of the guinea‐pig and human

The role of teratogens in neural crest development

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