Inflammatory stress in primary venous and aortic endothelial cells of type 1 diabetic mice.
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.
Bucciarelli
Loredana G
LG
IRCCS Istituto Clinico Humanitas, Via Manzoni 56, Rozzano 20089, Milan, Italy.
Pollreisz
Andreas
A
Kebschull
Moritz
M
Ganda
Anjali
A
Kalea
Anastasia Z
AZ
Hudson
Barry I
BI
Zou
Yu Shan
YS
Lalla
Evanthia
E
Ramasamy
Ravichandran
R
Colombo
Paolo C
PC
Schmidt
Ann Marie
AM
Yan
Shi Fang
SF
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
D018836:Inflammation Mediators; D053583:Interleukin-1beta; D012333:RNA, Messenger; D020170:Caspase 1