Processes Underlying the Nutritional Programming of Embryonic Development by Iron Deficiency in the Rat 英文参考文献.docVIP

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Processes Underlying the Nutritional Programming of Embryonic Development by Iron Deficiency in the Rat 英文参考文献.doc

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Processes Underlying the Nutritional Programming of Embryonic Development by Iron Deficiency in the Rat 英文参考文献

ProcessesUnderlyingtheNutritionalProgrammingof EmbryonicDevelopmentbyIronDeficiencyintheRat AngelinaSwali1*,SarahMcMullen1,HelenHayes2,LorraineGambling2,HarryJ.McArdle2, SimonC.Langley-Evans1 1SchoolofBiosciences,UniversityofNottingham,SuttonBonington,Loughborough,UnitedKingdom,2RowettInstituteofNutritionandHealth,UniversityofAberdeen, Aberdeen,UnitedKingdom Abstract Poor iron status is a global health issue, affecting two thirds of the world population to some degree. It is a particular problemamongpregnantwomen,inbothdevelopedanddevelopingcountries.Feedingpregnantratsadietdeficientin iron is associated with both hypertension and reduced nephron endowment in adult male offspring. However, the mechanistic pathway leading from iron deficiency to fetal kidney development remains elusive. This study aimed to establishtheunderlyingprocessesassociatedwithirondeficiencybyassessinggeneandproteinexpressionchangesinthe ratembryo,focussingontheresponsesoccurringatthetimeofthenutritionalinsult.Analysisofmicroarraydatashowed thatirondeficiencyinuteroresultedinthesignificantup-regulationof979genesanddown-regulationof1545genesin maleratembryos(d13).Affectedprocessesassociatedwiththesegenesincludedtheinitiationofmitosis,BAD-mediated apoptosis,theassemblyofRNApolymeraseIIpreinitiationcomplexesandWNTsignalling.Proteomicanalyseshighlighted7 proteins demonstrating significant up-regulation with iron deficiency and the down-regulation of 11 proteins. The main functionsofthesekeyproteinsincludedcellproliferation,proteintransportandfolding,cytoskeletalremodellingandthe proteasome complex. In line with our recent work, which identified the perturbation of the proteasome complex as ageneralisedresponsetoinuteromalnutrition,weproposethatirondeficiencyaloneleadstoamorespecificfailurein correct protein folding and transport. Such an imbalance in this delicate quality-control system can lead to cellular dysfunctionandapoptosis.Thereforethesefindingsofferaninsightintotheunderlyingmechanismsas