Chung-Ming Chen1, Hsiu-Chu Chou2, Liang-Ti Huang3. 1. 1] Department of Pediatrics, Taipei Medical University Hospital, Taipei, Taiwan [2] Department of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. 2. Department of Anatomy, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. 3. Department of Pediatrics, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Abstract
BACKGROUND: Maternal tobacco smoke exposure adversely affected fetal kidney development. Nicotine stimulates epithelial-mesenchymal transition and connective tissue growth factor (CTGF) expression in the renal epithelium. We hypothesized that maternal nicotine exposure would induce kidney fibrosis and involve CTGF in newborn rats. METHODS: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/d from gestational days 7-21 and gestational day 7 to postnatal day 14. A control group was injected with normal saline. Neonatal kidney tissues underwent histological analysis, collagen measurement, and western blot analysis. RESULTS: Tubular injury scores and total collagen contents were significantly higher in rats born to nicotine-treated dams than in rats born to normal saline-treated dams on postnatal days 7 and 21. Masson's trichrome staining further verified the presence of kidney fibrosis. Prenatal and/or postnatal nicotine exposure increased CTGF expression on postnatal days 7 and 21. CONCLUSION: Maternal nicotine exposure during gestation and lactation induces neonatal kidney fibrosis, and CTGF may be involved in the pathogenesis of kidney fibrosis. These results may be relevant to premature low-birth-weight infants who are conveyed a high risk of developing chronic kidney disease and exposed to breast milk of smoking mothers during the neonatal period.
BACKGROUND: Maternal tobacco smoke exposure adversely affected fetal kidney development. Nicotine stimulates epithelial-mesenchymal transition and connective tissue growth factor (CTGF) expression in the renal epithelium. We hypothesized that maternal nicotine exposure would induce kidney fibrosis and involve CTGF in newborn rats. METHODS:Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/d from gestational days 7-21 and gestational day 7 to postnatal day 14. A control group was injected with normal saline. Neonatal kidney tissues underwent histological analysis, collagen measurement, and western blot analysis. RESULTS:Tubular injury scores and total collagen contents were significantly higher in rats born to nicotine-treated dams than in rats born to normal saline-treated dams on postnatal days 7 and 21. Masson's trichrome staining further verified the presence of kidney fibrosis. Prenatal and/or postnatal nicotine exposure increased CTGF expression on postnatal days 7 and 21. CONCLUSION: Maternal nicotine exposure during gestation and lactation induces neonatal kidney fibrosis, and CTGF may be involved in the pathogenesis of kidney fibrosis. These results may be relevant to premature low-birth-weight infants who are conveyed a high risk of developing chronic kidney disease and exposed to breast milk of smoking mothers during the neonatal period.
Authors: Cagri Camsari; Joseph K Folger; Devin McGee; Steven J Bursian; Hongbing Wang; Jason G Knott; George W Smith Journal: Environ Health Perspect Date: 2016-11-04 Impact factor: 9.031
Authors: Vladimir Mayorov; Peter Uchakin; Venkataraman Amarnath; Alexander V Panov; Christy C Bridges; Roman Uzhachenko; Bill Zackert; Christy S Moore; Sean Davies; Anna Dikalova; Sergey Dikalov Journal: Redox Biol Date: 2019-08-14 Impact factor: 11.799