POSTER SESSION 3

Purpose: Pregnancy is a physiological model of adaptive and reversible heart enlargement. The molecular mechanisms determining physiological, non-pathological, heart enlargement are poorly known. Here we analyzed the role of the transcription factor C/EBPb in the development of pregnancy-induced cardiac hypertrophy. Methods:WeusedamodelofC/EBPbhaploinsufficiency(C/EBPb+/-)inmicetodeterminetherole ofC/EBPbinheartadaptationstopregnancy.Wild-type(Wt)andC/EBPb+/-pregnantmiceatday18 ofgestationweresacrificed,non-pregnantmiceofthetwogenotypesatsimilarageservedascontrols. Heartwasdissectedandprocessedformicroscopyanalysis,andfrozenforfurthermoleculardeterminations. Blood was collected and glucose and triglyceride levels were measured. Plasma was used for analysis of hormonal and cytokine profile (insulin, leptin, MCP-1, interleukin-6, resistin) employing Multiplex. qPCR was used to determine gene expression levels. Results: C/EBPb expression was increased in heart from Wt pregnant mice. Expression of other C/EBP subtypes (aandd)wasnot affected bygestation. C/EBPb+/-mice expressedC/EBPbproteins tolevelsclosetoone-halfthoseinWt.Pregnancy-inducedchangesinsystemicmetabolicandhormonal profiles were not essentially different in WTs versus C/EBPb+/- mice. C/EBPb+/- mice developed pregnancy-induced heart hypertrophy (heart weight to tibia length ratio) to a lower extent relative to Wt mice. The increase in cardiomyocyte size observed in pregnant Wt mice did not occur in pregnant C/EBPb+/- mice. The expression of marker genes of pathological cardiac hypertrophy, such as ANF and actinin, were unaltered due to pregnancy or to C/EBPb haploinsufficiency. Genes involved inglucose(GLUT1and GLUT4transporters),andfattyacid (medium chainacyl-CoA dehydrogenase) metabolism tended to be less expressed in hearts from C/EBPb+/- mice. Among gene markers of inflammation whose expression was analyzed in heart, interleukin-6 (IL-6) showed a marked differential