title: Alteration of embryonic AT(2)-R and inflammatory cytokines gene expression induced by prenatal exposure to lipopolysaccharide affects renal development.
abstract: Prenatal exposure to LPS(lipopolysaccharide) results in renal damage in offspring rats, but the mechanism is unknown. The present study was to explore the role of angiotensin II and inflammation in the development of renal damage induced by prenatal exposure to LPS. The pregnant rats were randomly divided into two groups, i.e., control group, LPS group. The rats in the two groups were administered intraperitoneally with vehicle or 0.79 mg/kg LPS on 8th, 10th and 12th day during gestation. The mRNA expression of angiotensinogen, renin, AT(1)-R, AT(2)-R, TNF-α and IL-6 in embryos were assessed. Renal Ang II-positive cells, monocytes/macrophages, lymphocytes, collagen I and TUNEL-positive cells were identified by immunohistochemical staining in newborn and 7-week-old offspring rats. The number of glomeruli and creatinine clearance rate were determined in offspring at 7 weeks of age. The results showed that prenatal LPS decreased AT(2)-R mRNA expression but increased TNF-α and IL-6 mRNA expression in embryos. Prenatal LPS decreased renal angiotensin II-positive cells in newborn offspring rats, while these increased in 7-week-old offspring rats. Prenatal LPS decreased glomerular number and creatinine clearance rate but increased renal infiltrating monocytes/macrophages and lymphocytes at 7 weeks of age. Prenatal LPS also increased TUNEL-positive cells and collagen I expressions in newborn rats and 7-week-old offspring rats.
  
  
  CONCLUSIONS
  Alteration of embryonic AT(2)-R and inflammatory cytokines gene expression induced by prenatal exposure to lipopolysaccharide affects renal development.
authors.affiliation: Department of Pharmacology, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471003, China. haohaoxq@tom.com
authors.forename: Xue-Qin
authors.initials: XQ
authors.lastname: Hao
authors.forename: Tao
authors.initials: T
authors.lastname: Kong
authors.forename: Shou-Yan
authors.initials: SY
authors.lastname: Zhang
authors.forename: Zhen-Sheng
authors.initials: ZS
authors.lastname: Zhao
mesh_terms: D000804:Angiotensin II; D000818:Animals; D017209:Apoptosis; D016207:Cytokines / Q000378:metabolism; D004622:Embryo, Mammalian; D005260:Female; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects / Q000196:embryology* / Q000503:physiopathology; D007677:Kidney Function Tests; D008070:Lipopolysaccharides / Q000633:toxicity; D020411:Oligonucleotide Array Sequence Analysis; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D044139:Receptor, Angiotensin, Type 2; D000804:Angiotensin II