RGD Reference Report - Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring. - Rat Genome Database

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Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring.

Authors: Xiao, DaLiao  Wang, Lei  Huang, Xiaohui  Li, Yong  Dasgupta, Chiranjib  Zhang, Lubo 
Citation: Xiao D, etal., PLoS One. 2016 Feb 26;11(2):e0150557. doi: 10.1371/journal.pone.0150557. eCollection 2016.
RGD ID: 13792772
Pubmed: PMID:26918336   (View Abstract at PubMed)
PMCID: PMC4769226   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0150557   (Journal Full-text)

Fetal nicotine exposure increased risk of developing cardiovascular disease later in life. The present study tested the hypothesis that perinatal nicotine-induced programming of heart ischemia-sensitive phenotype is mediated by enhanced reactive oxygen species (ROS) in offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in drinking water. Experiments were conducted in 8 month old age male offspring. Isolated hearts were perfused in a Langendorff preparation. Perinatal nicotine treatment significantly increased ischemia and reperfusion-induced left ventricular injury, and decreased post-ischemic recovery of left ventricular function and coronary flow rate. In addition, nicotine enhanced cardiac ROS production and significantly attenuated protein kinase Ce (PKCe) protein abundance in the heart. Although nicotine had no effect on total cardiac glycogen synthase kinase-3ß (GSK3ß) protein expression, it significantly increased the phosphorylation of GSK3ß at serine 9 residue in the heart. NAC inhibited nicotine-mediated increase in ROS production, recovered PKCe gene expression and abrogated increased phosphorylation of GSK3ß. Of importance, NAC blocked perinatal nicotine-induced increase in ischemia and reperfusion injury in the heart. These findings provide novel evidence that increased oxidative stress plays a causal role in perinatal nicotine-induced developmental programming of ischemic sensitive phenotype in the heart, and suggest potential therapeutic targets of anti-oxidative stress in the treatment of ischemic heart disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GSK3BHumanMyocardial Reperfusion Injury treatmentISOGsk3b (Rattus norvegicus) RGD 
Gsk3bRatMyocardial Reperfusion Injury treatmentIDA  RGD 
Gsk3bMouseMyocardial Reperfusion Injury treatmentISOGsk3b (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gsk3b  (glycogen synthase kinase 3 beta)

Genes (Mus musculus)
Gsk3b  (glycogen synthase kinase 3 beta)

Genes (Homo sapiens)
GSK3B  (glycogen synthase kinase 3 beta)


Additional Information