Maternal nicotine exposure induces epithelial-mesenchymal transition in rat offspring lungs

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Abstract

Background: Maternal nicotine exposure induces lung injuries and fibrosis in rat offspring. Epithelial-mesenchymal transition (EMT) following lung injury is a process in which epithelial cells mediate tissue repair. Objective: To determine the effects of maternal nicotine exposure on EMT in neonatal rat lungs. Methods: Nicotine was administered to pregnant Sprague-Dawley rats using a subcutaneous osmotic minipump that delivered a dose of 6 mg/kg/day on gestational days 7-21 or from gestational day 7 to postnatal day 14. A control group received an equal volume of saline. Results: The percentage of 8-hydroxy-2'-deoxyguanosine-positive cells in nuclear staining was significantly higher, the E-cadherin protein expression was significantly lower, and the N-cadherin protein expression was significantly higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal day 7. These characteristics of EMT were associated with a significant increase in α-smooth muscle actin (SMA) expression on postnatal day 21. Rats born to prenatal and postnatal nicotine-treated dams showed significantly higher α-SMA expression and total collagen than those born to prenatal saline- and nicotine-treated dams on postnatal day 21. The number of cells expressing fibroblast-specific protein 1 and vimentin was higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal days 7 and 21. Conclusions: Maternal nicotine exposure during gestation and lactation induces EMT and contributes to lung fibrosis in rat offspring.

Original languageEnglish
Pages (from-to)179-187
Number of pages9
JournalNeonatology
Volume108
DOIs
Publication statusPublished - Sep 18 2015

Fingerprint

Maternal Exposure
Epithelial-Mesenchymal Transition
Nicotine
Lung
Lung Injury
Cadherins
Smooth Muscle
Actins
Fibrosis
Vimentin
Lactation
Sprague Dawley Rats
Proteins
Collagen
Cell Count
Epithelial Cells
Staining and Labeling

Keywords

  • E-cadherin
  • Fibroblast-specific protein 1
  • N-cadherin
  • Nicotine
  • α-Smooth muscle actin

ASJC Scopus subject areas

  • Developmental Biology
  • Pediatrics, Perinatology, and Child Health

Cite this

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title = "Maternal nicotine exposure induces epithelial-mesenchymal transition in rat offspring lungs",
abstract = "Background: Maternal nicotine exposure induces lung injuries and fibrosis in rat offspring. Epithelial-mesenchymal transition (EMT) following lung injury is a process in which epithelial cells mediate tissue repair. Objective: To determine the effects of maternal nicotine exposure on EMT in neonatal rat lungs. Methods: Nicotine was administered to pregnant Sprague-Dawley rats using a subcutaneous osmotic minipump that delivered a dose of 6 mg/kg/day on gestational days 7-21 or from gestational day 7 to postnatal day 14. A control group received an equal volume of saline. Results: The percentage of 8-hydroxy-2'-deoxyguanosine-positive cells in nuclear staining was significantly higher, the E-cadherin protein expression was significantly lower, and the N-cadherin protein expression was significantly higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal day 7. These characteristics of EMT were associated with a significant increase in α-smooth muscle actin (SMA) expression on postnatal day 21. Rats born to prenatal and postnatal nicotine-treated dams showed significantly higher α-SMA expression and total collagen than those born to prenatal saline- and nicotine-treated dams on postnatal day 21. The number of cells expressing fibroblast-specific protein 1 and vimentin was higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal days 7 and 21. Conclusions: Maternal nicotine exposure during gestation and lactation induces EMT and contributes to lung fibrosis in rat offspring.",
keywords = "E-cadherin, Fibroblast-specific protein 1, N-cadherin, Nicotine, α-Smooth muscle actin",
author = "Chen, {Chung Ming} and Chou, {Hsiu Chu} and Huang, {Liang Ti}",
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T1 - Maternal nicotine exposure induces epithelial-mesenchymal transition in rat offspring lungs

AU - Chen, Chung Ming

AU - Chou, Hsiu Chu

AU - Huang, Liang Ti

PY - 2015/9/18

Y1 - 2015/9/18

N2 - Background: Maternal nicotine exposure induces lung injuries and fibrosis in rat offspring. Epithelial-mesenchymal transition (EMT) following lung injury is a process in which epithelial cells mediate tissue repair. Objective: To determine the effects of maternal nicotine exposure on EMT in neonatal rat lungs. Methods: Nicotine was administered to pregnant Sprague-Dawley rats using a subcutaneous osmotic minipump that delivered a dose of 6 mg/kg/day on gestational days 7-21 or from gestational day 7 to postnatal day 14. A control group received an equal volume of saline. Results: The percentage of 8-hydroxy-2'-deoxyguanosine-positive cells in nuclear staining was significantly higher, the E-cadherin protein expression was significantly lower, and the N-cadherin protein expression was significantly higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal day 7. These characteristics of EMT were associated with a significant increase in α-smooth muscle actin (SMA) expression on postnatal day 21. Rats born to prenatal and postnatal nicotine-treated dams showed significantly higher α-SMA expression and total collagen than those born to prenatal saline- and nicotine-treated dams on postnatal day 21. The number of cells expressing fibroblast-specific protein 1 and vimentin was higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal days 7 and 21. Conclusions: Maternal nicotine exposure during gestation and lactation induces EMT and contributes to lung fibrosis in rat offspring.

AB - Background: Maternal nicotine exposure induces lung injuries and fibrosis in rat offspring. Epithelial-mesenchymal transition (EMT) following lung injury is a process in which epithelial cells mediate tissue repair. Objective: To determine the effects of maternal nicotine exposure on EMT in neonatal rat lungs. Methods: Nicotine was administered to pregnant Sprague-Dawley rats using a subcutaneous osmotic minipump that delivered a dose of 6 mg/kg/day on gestational days 7-21 or from gestational day 7 to postnatal day 14. A control group received an equal volume of saline. Results: The percentage of 8-hydroxy-2'-deoxyguanosine-positive cells in nuclear staining was significantly higher, the E-cadherin protein expression was significantly lower, and the N-cadherin protein expression was significantly higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal day 7. These characteristics of EMT were associated with a significant increase in α-smooth muscle actin (SMA) expression on postnatal day 21. Rats born to prenatal and postnatal nicotine-treated dams showed significantly higher α-SMA expression and total collagen than those born to prenatal saline- and nicotine-treated dams on postnatal day 21. The number of cells expressing fibroblast-specific protein 1 and vimentin was higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal days 7 and 21. Conclusions: Maternal nicotine exposure during gestation and lactation induces EMT and contributes to lung fibrosis in rat offspring.

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KW - Nicotine

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