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Inflammatory stress in primary venous and aortic endothelial cells of type 1 diabetic mice

IRCCS Istituto Clinico Humanitas,Via Manzoni 56, Rozzano 20089, Milan, Italy

Andreas Pollreisz

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA, College of Dental Medicine, Columbia University Medical Center, New York 10032, USA

Moritz Kebschull

College of Dental Medicine, Columbia University Medical Center, New York 10032, USA

Anjali Ganda

Department of Medicine, Columbia University Medical Center, New York 10032, USA

Anastasia Z. Kalea

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA

Barry I. Hudson

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA

Yu Shan Zou

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA

Evanthia Lalla

College of Dental Medicine, Columbia University Medical Center, New York 10032, USA

Ravichandran Ramasamy

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA

Paolo C. Colombo

Department of Medicine, Columbia University Medical Center, New York 10032, USA

Ann Marie Schmidt

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA

Shi Fang Yan

Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York 10032, USA, sy18{at}columbia.edu

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.

Method: 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.

Conclusion: These data suggest that diabetes imparts diffuse endothelial perturbation in the arterial and venous endothelium.

Key Words: vein • artery • endothelium • inflammation • diabetes

Diabetes and Vascular Disease Research, Vol. 6, No. 4, 249-261 (2009)
DOI: 10.1177/1479164109338775


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