Metallothionein-I- and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction

Selvaratnam, Johanna; Guan, Haiyan; Koropatnick, James; Yang, Kaiping

doi:10.1152/ajpendo.00157.2013

Cited by 23 publications

(12 citation statements)

References 65 publications

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“…Using a rocking microtome, the lungs were carefully sectioned; 5 μm sections were transferred to Superfrost/Plus microscope slides (Fisher Scientific, Whitby, ON, Canada). Sections were stained using a standard hematoxylin and eosin protocol (29). Selected lung sections were also stained with periodic acid‐Schiff (PAS).…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis was used to determine various protein levels, as described previously (29). Briefly, lung tissues were homogenized in 10 volumes of ice‐cold 10 mM sodium phosphate buffer, pH 7.0, containing 0.25 M sucrose.…”

Section: Methodsmentioning

confidence: 99%

“…The relative abundance of various mRNAs was assessed by a 2-step real-time quantitative reverse transcriptase PCR (qRT-PCR), as described previously (29) with the following specific modifications. Briefly, total RNA was extracted from fetal lung tissues using RNeasy Mini Kit (Qiagen, Mississauga, ON, Canada) coupled with on-column DNase digestion with the RNase-Free DNase Set (Qiagen) according to the manufacturer's instructions.…”

Section: Real-time Quantitative Reverse Transcriptase Pcrmentioning

confidence: 99%

“…Western blot analysis was used to determine various protein levels, as described previously (29). Briefly, lung tissues were (continued from previous page) hypoxia-inducible factor; PAS, periodic acid-Schiff; PCNA, proliferating cell nuclear antigen; qRT-PCR, real-time quantitative reverse transcriptase PCR; Snx5, sorting nexin 5; SP, surfactant protein; Sp3, specificity protein 3; TTBS, Tween-20 in Tris-buffered saline homogenized in 10 volumes of ice-cold 10 mM sodium phosphate buffer, pH 7.0, containing 0.25 M sucrose.…”

Section: Western Blot Analysismentioning

confidence: 99%

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Prenatal exposure to bisphenol A disrupts mouse fetal lung development

et al. 2015

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Developmental exposure to bisphenol A (BPA) is associated with lung dysfunction and diseases. However, it is unknown if this association has a fetal origin. The present study addressed this important question by examining the effects of BPA on fetal lung development. BPA was administered to pregnant mice via diet from embryonic day (E) 7.5 to E18.5. Fetal lungs were analyzed at E18.5 for changes in structure and expression of key molecular markers of lung maturation. Our main findings were as follows: BPA severely retards fetal lung maturation, as evidenced by diminished alveolar airspace (15% of control) and thickened septa, hallmarks of lung immaturity; this immaturity is characterized by aberrant alveolar epithelial type I cell differentiation because expression of the type I cell marker, aquaporin 5, but not type II cell markers, is dramatically reduced (16% of control); and the effects of BPA are likely mediated through the glucocorticoid signaling pathway because the expression of epithelial sodium channel γ and glutathione peroxidase, 2 well-known glucocorticoid target genes, is down-regulated in BPA-exposed fetal lungs, and, importantly, maternal dexamethasone administration rescues the lung immaturity phenotype. Taken together, these findings demonstrate that BPA disrupts fetal lung maturation, thus suggesting a fetal origin for BPA-induced lung diseases.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Real-time Quantitative Reverse Transcriptase Pcrmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

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Prenatal exposure to bisphenol A disrupts mouse fetal lung development

et al. 2015

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“…In mice, maternal Cd exposure in mid-gestation resulted in a relatively specific forelimb ectrodactyly [20][21][22][23][24][25]. Moreover, maternal Cd exposure in middle and late gestational age induced FGR in mice [15,26,27]. Nevertheless, the molecular mechanism for Cd-induced FGR remains obscure.…”

Section: Introductionmentioning

confidence: 99%

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Wang

et al. 2016

Reproductive Toxicology

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Prenatal Exposure to Bisphenol A Disrupts Mouse Fetal Liver Maturation in a Sex-Specific Manner

2015

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Bisphenol A (BPA) is one of the most prevalent endocrine disrupting chemicals in the environment. Developmental exposure to BPA is known to be associated with liver dysfunction and diseases, such as hepatic steatosis, liver tumors, metabolic syndrome, and altered hepatic gene expression, and DNA methylation profiles. However, the effects of BPA on rodent liver development are unknown. The present study was undertaken to address this important question using the mouse as an experimental model. Pregnant mice were exposed to BPA via diet from embryonic day 7.5 (E7.5) to E18.5. At E18.5, fetal livers were collected, and analyzed for changes in the expression of key hepatocyte maturation markers. We found the following significant alterations in BPA-exposed female but not male fetal livers: (a) levels of the mature hepatocyte markers, albumin and glycogen synthase proteins, were decreased (-65% and -40%, respectively); (b) levels of the immature hepatocyte marker, α-fetoprotein, were increased (+43%); (c) the level of C/EBP-α protein, the master transcription factor essential for hepatocyte maturation, was down-regulated (-50%); and (d) the level of PCNA protein (marker of proliferation) was elevated (+40%), while that of caspase-3 protein and activity (markers of apoptosis) was reduced (-40% and -55%, respectively), suggestive of a perturbed balance between cell proliferation and apoptosis in BPA-exposed female fetuses. Taken together, these findings demonstrate that prenatal exposure to BPA disrupts the mouse fetal liver maturation in a sex-specific manner, and suggest a fetal origin for BPA-induced hepatic dysfunction and diseases.

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Metallothionein-I- and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction

Abstract: nein-I-and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction.

Cited by 23 publications

References 65 publications

Prenatal exposure to bisphenol A disrupts mouse fetal lung development

Prenatal exposure to bisphenol A disrupts mouse fetal lung development

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Prenatal Exposure to Bisphenol A Disrupts Mouse Fetal Liver Maturation in a Sex-Specific Manner

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