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Analysis of Physiologic E-Selectin-Mediated Leukocyte Rolling on Microvascular Endothelium
Published on: February 11, 2009
High glucose-treated macrophages augment E-selectin expression in endothelial cells.
Te-Chuan Chen1, Shao-Ju Chien, Hsing-Chun Kuo
1Division of Nephrology, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
The Journal of Biological Chemistry
|June 11, 2011
Summary
High glucose conditions activate macrophages, increasing E-selectin expression in endothelial cells via JNK, p38 MAPK, NF-κB, and AP-1 pathways. This macrophage-driven E-selectin may accelerate arterial disease in diabetes.
Area of Science:
- Vascular biology
- Immunology
- Endocrinology
Background:
- E-selectin expression on endothelial cells (ECs) is vital for leukocyte recruitment during inflammation.
- Type 2 diabetes mellitus is characterized by macrophage accumulation and elevated serum E-selectin.
- The precise interactions between macrophages and ECs in regulating vascular function, especially in diabetes, remain unclear.
Purpose of the Study:
- To investigate how high glucose (HG)-treated macrophages modulate EC E-selectin expression.
- To elucidate the molecular mechanisms involved in this process.
Main Methods:
- Prepared conditioned media from HG-treated macrophages (HG-MCM).
- Stimulated ECs with HG-MCM and assessed E-selectin expression.
- Utilized pathway inhibitors, small interfering RNAs (siRNAs), transcription factor ELISAs, chromatin immunoprecipitation, protein arrays, and neutralizing antibodies.
Main Results:
- HG-MCM significantly increased EC E-selectin expression and secretion.
- Activation of JNK and p38 MAPK pathways in ECs was critical for this induction.
- HG-MCM enhanced NF-κB and AP-1 DNA-binding activity in ECs, which was necessary for E-selectin expression.
- Macrophage inflammatory protein 1α and 1β were identified as key mediators.
Conclusions:
- Macrophage-derived factors, particularly MIP-1α/β, induce E-selectin expression in ECs under high glucose conditions.
- The JNK, p38 MAPK, NF-κB, and AP-1 signaling pathways are essential mediators of this effect.
- Elevated E-selectin, stimulated by macrophages in a high glucose environment, may contribute to atherogenesis and accelerate vascular disease in diabetes.
