title: Sexual dimorphism in gene expression after aneurysmal subarachnoid hemorrhage.
abstract: OBJECTIVE
  Inflammation and compromise in structure and function of cerebral parenchymal microvasculature begins early after subarachnoid hemorrhage (SAH). We recently found greater inflammation and greater vascular compromise in male than in female rats following SAH. In this study, we investigated whether this cross-sexual difference in pathology is reflected in expression levels of genes related to vascular inflammation and structural compromise.
  
  
  METHODS
  Age-matched male and female rats underwent sham surgery or SAH by endovascular perforation. Early physiology (intracranial pressure (ICP), blood pressure (BP), heart rate, and cerebral blood flow) was monitored. Cerebral RNA was extracted at sacrifice 3 h after surgery and assayed for expression of thrombomodulin (Thbd), endothelial nitric oxide synthase (eNos;Nos3), intracellular adhesion molecule-1 (Icam1), vascular endothelial growth factor (Vegf), interleukin-1beta (Il1β) tumor necrosis factor-alpha (Tnf-α), and arginine vasopressin (Avp).
  
  
  RESULTS
  Increases in ICP and BP at SAH appeared slightly greater in males but the difference did not reach statistical difference, indicating that SAH intensity did not differ significantly between the sexes. Of the seven genes studied two; Tnf-α and Vegf, did not change after injury, while the remainder showed significant responses to SAH. Response of Nos3 and Thbd was markedly different between the sexes, with expression greater in males.
  
  
  CONCLUSIONS
  This study finds that sexual dimorphism is present in the response of some but not all genes to SAH. Since products of genes exhibiting sexual dimorphism have anti-inflammatory activities, our results indicate that previously found sex-based differences in vascular pathology are paralleled by sexually dimorphic changes in gene expression following SAH.
authors.affiliation: a Department of Neurosurgery, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
authors.forename: Victor
authors.initials: V
authors.lastname: Friedrich
authors.forename: Weina
authors.initials: W
authors.lastname: Bi
authors.forename: Fatima A
authors.initials: FA
authors.lastname: Sehba
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000235:genetics / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D007427:Intracranial Pressure; D008297:Male; D010751:Phosphopyruvate Hydratase / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012727:Sex Characteristics; D013345:Subarachnoid Hemorrhage / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D018180:Thrombomodulin / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D018180:Thrombomodulin; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D001127:Arginine Vasopressin; D018799:Intercellular Adhesion Molecule-1; D010751:Phosphopyruvate Hydratase
keywords: Early brain injury; Gender; Inflammation; Stroke; Vascular pathology