title: In utero exposure to maternal diabetes impairs vascular expression of prostacyclin receptor in rat offspring.
abstract: OBJECTIVE
  To evaluate modifications of arterial structure, gene expression, and function in our model of rats exposed to maternal diabetes.
  
  
  METHODS
  Morphometric analyses of elastic vessels structure and determination of thoracic aortic gene expression profile with oligonucleotide chips (Agilent, G4130, 22k) were performed before the onset of established hypertension (3 months).
  
  
  RESULTS
  Arterial parameters of in situ fixed thoracic aorta were not significantly different between control mother offspring and diabetic mother offspring (DMO). The aortic gene expression profile of DMO is characterized by modifications of several members of the arachidonic acid metabolism including a twofold underexpression of prostacyclin receptor, which could contribute to decreased vasodilatation. This was confirmed by ex vivo experiments on isolated aortic rings. Pharmacological studies on conscious rats showed that systolic blood pressure decline in response to a PGI(2) analog was impaired in DMO rats.
  
  
  CONCLUSIONS
  These results suggest an abnormal vascular fetal programming of prostacyclin receptor in rats exposed in utero to maternal hyperglycemia that is associated with impaired vasodilatation and may be involved in the pathophysiology of hypertension in this model.
authors.affiliation: NSERM U872, Centre de Recherche des Cordeliers, Universite's Pierre et Marie Curie et Paris-Descartes, Paris, France. celine.fassot@inserm.fr
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Duong Van Huyen
authors.forename: Emilie
authors.initials: E
authors.lastname: Vessières
authors.forename: Claudine
authors.initials: C
authors.lastname: Perret
authors.forename: Adrien
authors.initials: A
authors.lastname: Troise
authors.forename: Sonia
authors.initials: S
authors.lastname: Prince
authors.forename: Anne-Laure
authors.initials: AL
authors.lastname: Guihot
authors.forename: Pascal
authors.initials: P
authors.lastname: Barbry
authors.forename: Daniel
authors.initials: D
authors.lastname: Henrion
authors.forename: Patrick
authors.initials: P
authors.lastname: Bruneval
authors.forename: Stéphane
authors.initials: S
authors.lastname: Laurent
authors.forename: Martine
authors.initials: M
authors.lastname: Lelièvre-Pégorier
authors.forename: Céline
authors.initials: C
authors.lastname: Fassot
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000196:embryology / Q000502:physiology; D016718:Arachidonic Acid / Q000378:metabolism; D001794:Blood Pressure; D018076:DNA, Complementary / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D020411:Oligonucleotide Array Sequence Analysis; D011247:Pregnancy; D011248:Pregnancy Complications / Q000235:genetics / Q000503:physiopathology*; D012313:RNA / Q000235:genetics / Q000302:isolation & purification; D051381:Rats; D017207:Rats, Sprague-Dawley; D044006:Receptors, Epoprostenol / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014664:Vasodilation
chemical_list: D018076:DNA, Complementary; D044006:Receptors, Epoprostenol; D016718:Arachidonic Acid; D012313:RNA