A Diabetic Microvascular Whole Blood Flow Model as a New Tool to Study Diabetes-Associated Thrombotic Complications
ISTH Academy. Schroeder V. Jul 9, 2019; 264351; PB1157 Topic: Cardiovascular Risk Factors
Verena Schroeder
Verena Schroeder
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A Diabetic Microvascular Whole Blood Flow Model as a New Tool to Study Diabetes-associated Thrombotic Complications

L. Jenny1, A. Melmer2, M. Laimer2, W. Lam3,4, V. Schroeder1
1University of Bern, Department for BioMedical Research, Bern, Switzerland, 2University Hospital Bern, University Clinic for Diabetology, Endocrinology, Nutrition & Metabolism, Bern, Switzerland, 3Georgia Institute of Technology, Wallace H. Coulter Department of Biomedical Engineering, Atlanta, United States, 4Emory University, Atlanta, United States

Main Topic: Arterial Thromboembolism
Category: Cardiovascular Risk Factors

Background: Diabetes is a proinflammatory and prothrombotic condition with a high risk of atherothrombotic complications. Endothelial dysfunction, activation of blood cells, and changes in plasma proteins (including increased protein levels and non-enzymatic protein glycation) have been shown to contribute to the development of thrombotic complications. However, in vitro experiments mostly focused on individual aspects without taking into account the complex interactions between endothelial cells (ECs), blood cells and plasma proteins. Clinical studies often showed associations of certain biomarkers with a disease, but were not able to prove a causal relationship.
Aims: Our aim was to develop an in vitro system that reflects the in vivo situation as close as possible for the study of prothrombotic and proinflammatory changes that occur in diabetes and may promote thrombus formation.
Methods: Primary cardiac microvascular ECs from non-diabetic individuals (control cells) and from patients with type 1 (T1DM cells) or type 2 diabetes mellitus (T2DM cells) were obtained from Lonza. The ECs were seeded and grown to confluence in parallel channels of transparent silicone chips. Freshly drawn whole blood was obtained from healthy individuals or patients with T1DM or T2DM after informed consent, the study was approved by the local ethics committee. The chips coated with diabetic or control ECs were perfused with whole blood from diabetic patients or healthy donors at physiological flow rates. Clot formation within the channels was assessed by confocal microscopy by measuring the fluorescence signal of immobilised fibrin over time.
Results: Our results so far show that clot formation is clearly accelerated and increased in the presence of T2DM ECs and T2DM whole blood compared with control cells and non-diabetic blood.
Conclusions: Our model allows to study the complex mechanisms contributing to thrombus formation in diabetes. It may also represent a valuable tool to evaluate novel therapeutic approaches.

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