title: Inflammatory stress in primary venous and aortic endothelial cells of type 1 diabetic mice.
abstract: OBJECTIVE
  The progression of diabetes is associated with profound endothelial dysfunction. We tested the hypothesis that cellular stress would be detectable in ECs retrieved from arterial and venous vessels of diabetic mice.
  
  
  METHODS
  We describe a method for direct isolation of well-characterised aortic and venous ECs from mice in which cells are not subjected to propagation in culture.
  
  
  RESULTS
  Gene expression profiling, confirmed by real-time PCR, revealed a progressive increase in markers of injury within two main gene families, EC activation and EC apoptosis, in aortic and venous ECs recovered from diabetic versus non-diabetic mice. In short-term diabetes, Il1b mRNA transcripts were higher in aortic and venous ECs of diabetic mice versus controls. In long-term diabetes, casp-1 mRNA transcripts were higher in aortic and venous ECs of diabetic mice versus controls.
  
  
  CONCLUSIONS
  These data suggest that diabetes imparts diffuse endothelial perturbation in the arterial and venous endothelium.
authors.affiliation: IRCCS Istituto Clinico Humanitas, Via Manzoni 56, Rozzano 20089, Milan, Italy.
authors.forename: Loredana G
authors.initials: LG
authors.lastname: Bucciarelli
authors.forename: Andreas
authors.initials: A
authors.lastname: Pollreisz
authors.forename: Moritz
authors.initials: M
authors.lastname: Kebschull
authors.forename: Anjali
authors.initials: A
authors.lastname: Ganda
authors.forename: Anastasia Z
authors.initials: AZ
authors.lastname: Kalea
authors.forename: Barry I
authors.initials: BI
authors.lastname: Hudson
authors.forename: Yu Shan
authors.initials: YS
authors.lastname: Zou
authors.forename: Evanthia
authors.initials: E
authors.lastname: Lalla
authors.forename: Ravichandran
authors.initials: R
authors.lastname: Ramasamy
authors.forename: Paolo C
authors.initials: PC
authors.lastname: Colombo
authors.forename: Ann Marie
authors.initials: AM
authors.lastname: Schmidt
authors.forename: Shi Fang
authors.initials: SF
authors.lastname: Yan
mesh_terms: D000818:Animals; D001011:Aorta / Q000276:immunology* / Q000473:pathology; D017209:Apoptosis; D020170:Caspase 1 / Q000235:genetics; D002469:Cell Separation; D002478:Cells, Cultured; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D042783:Endothelial Cells / Q000276:immunology* / Q000473:pathology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D007249:Inflammation / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013312:Stress, Physiological / Q000235:genetics / Q000276:immunology*; D013997:Time Factors; D014682:Vena Cava, Inferior / Q000276:immunology* / Q000473:pathology
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D012333:RNA, Messenger; D020170:Caspase 1