Microarray analysis of murine limb bud ectoderm and mesoderm after exposure to cadmium or acetazolamide

Schreiner, Claire M.; Bell, Sheila M.; Scott, William J.

doi:10.1002/bdra.20577

Cited by 13 publications

(8 citation statements)

References 93 publications

(102 reference statements)

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“…Ethanol exposure induces postaxial forelimb ectrodactyly in the mouse (Chrisman et al, 2004), a finding that characterizes Shh-null mice (Chiang et al, 2001). It has been suggested that an ethanol-induced APR results in embryonic zinc deficiency and reduces Shh signaling leading to subsequent dysmorphology (Schreiner et al, 2009).…”

Section: Cell-signaling Cascadesmentioning

confidence: 99%

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Uriu‐Adams

Keen

2010

Birth Defects Research Pt B

118

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A large body of evidence supports the concept that human pregnancy outcome is significantly influenced by the nutritional status of the mother. The consumption of "poor diets" has been associated with an increased risk for pregnancy complications, including gross structural birth defects, prematurity, low birth weight, and an increased risk for neurobehavioral and immunological abnormalities after birth. Forty-four years ago, zinc deficiency in mammals was shown to be teratogenic. Maternal zinc deficiency produces effects ranging from infertility and embryo/fetal death, to intrauterine growth retardation and teratogenesis. Postnatal complications of maternal zinc deficiency can also occur, and include behavioral abnormalities, impaired immunocompetence, and an elevated risk for high blood pressure in the offspring. It has been suggested that developmental zinc deficiency in humans can present a significant challenge to the conceptus, increasing the risk for numerous defects. Developmental zinc deficiency can occur through multiple pathways, and the concept that acute phase response-induced changes in maternal zinc metabolism may be a common cause of embryonic and fetal zinc deficiency is presented. Potential mechanisms underlying the teratogenic effects of zinc deficiency are reviewed. The potential value of maternal zinc supplementation in high risk pregnancies is discussed.

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Section: Cell-signaling Cascadesmentioning

confidence: 99%

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Uriu‐Adams

Keen

2010

Birth Defects Research Pt B

118

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“…Shh is a Zn‐dependent developmental trigger [57], and reduced Shh expression has been implicated in ethanol‐induced postaxial forelimb ectrodactyly in the mouse [58]. Schreiner et al [59] have suggested that a state of embryonic Zn deficiency secondary to an alcohol‐induced acute‐phase response (APR) (see below [60–62]) in the mother results in reduced Shh signaling with subsequent dysmorphology [59]. This is an interesting hypothesis that merits further investigation.…”

Section: Alcohol–zn Interactionsmentioning

confidence: 99%

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

Keen

Uriu‐Adams

Skalny³

et al. 2010

BioFactors

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There is increasing evidence that human pregnancy outcome can be significantly compromised by suboptimal maternal nutritional status. Poor diet results in a maternal-fetal environment in which the teratogenicity of other insults such as alcohol might be amplified. As an example, there is evidence that zinc (Zn) can interact with maternal alcohol exposure to influence the risk for fetal alcohol spectrum disorders (FASD). Studies with experimental animals have shown that the teratogenicity of alcohol is increased under conditions of Zn deficiency, while its teratogenicity is lessened when animals are given Zn supplemented diets or Zn injections prior to the alcohol exposure. Alcohol can precipitate an acute phase response resulting in a subsequent increase in maternal liver metallothionein, which can sequester Zn and lead to decreased Zn transfer to the fetus. Importantly, the teratogenicity of acute alcohol exposure is reduced in metallothionein knockout mice, which can have improved Zn transfer to the conceptus relative to wild-type mice. Consistent with the above, Zn status has been reported to be low in alcoholic women at delivery. Preliminary data from two basic science and clinical nutritional studies that are ongoing as part of the international Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD) support the potential role of Zn, among other nutritional factors, relative to risk for FASD. Importantly, the nutrient levels being examined in these studies are relevant to general clinical populations and represent suboptimal levels rather than severe deficiencies. These data suggest that moderate deficiencies in single nutrients can act as permissive factors for FASD, and that adequate nutritional status or intervention through supplementation may provide protection for some of the effects of prenatal alcohol exposure.

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“…Several teratogens induce right-dominant, postaxial ectrodactyly in mouse forelimbs (i.e., an almost perfect phenocopy of the R Low /- mutant) when the animals are exposed to these agents around E9.5 (Bell et al, 2005; Schreiner et al, 2009). Interestingly, some of the teratogens, e.g., cadmium and ethanol, down-regulate endogenous Reck in ATDC5 cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…A variety of teratogens, including cadmium, acetazolamide, and ethanol, are known to induce a common limb malformation in mice after treatment at E9.5 (Bell et al, 2005; Schreiner et al, 2009). This malformation (postaxial, right-dominant forelimb ectrodactyly) is almost a perfect phenocopy of R Low /- mice.…”

Section: Discussionmentioning

confidence: 99%

The transformation suppressor gene Reck is required for postaxial patterning in mouse forelimbs

Yamamoto¹,

Matsuzaki²,

Takahashi

et al. 2012

Biology Open

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SummaryThe membrane-anchored metalloproteinase-regulator RECK has been characterized as a tumor suppressor. Here we report that mice with reduced Reck-expression show limb abnormalities including right-dominant, forelimb-specific defects in postaxial skeletal elements. The forelimb buds of low-Reck mutants have an altered dorsal ectoderm with reduced Wnt7a and Igf2 expression, and hypotrophy in two signaling centers (i.e., ZPA and AER) that are essential for limb outgrowth and patterning. Reck is abundantly expressed in the anterior mesenchyme in normal limb buds; mesenchyme-specific Reck inactivation recapitulates the low-Reck phenotype; and some teratogens downregulate Reck in mesenchymal cells. Our findings illustrate a role for Reck in the mesenchymal-epithelial interactions essential for mammalian development.

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Microarray analysis of murine limb bud ectoderm and mesoderm after exposure to cadmium or acetazolamide

Abstract: We propose that these two teratogens and others (valproic acid and ethanol) lower sonic hedgehog signaling by perturbation of zinc function in the sonic hedgehog protein.

Cited by 13 publications

References 93 publications

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

The transformation suppressor gene Reck is required for postaxial patterning in mouse forelimbs

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