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Pulsatile versus oscillatory shear stress regulates NADPH oxidase subunit expression: implication for native LDL
Juliana Hwang1, Michael H Ing, Adler Salazar
1Department of Biomedical Engineering and Division of Cardiovascular Medicine, University of Southern California, Los Angeles, Calif, USA.
Circulation Research
|November 1, 2003
Summary
Oscillating shear stress increases reactive oxygen species and modifies low-density lipoprotein (LDL), promoting inflammation. Conversely, pulsatile flow reduces these effects, highlighting shear stress
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Function
- Biochemistry
Background:
- Shear stress influences endothelial cells, affecting nitric oxide and superoxide production.
- The role of shear stress in regulating reactive species, low-density lipoprotein (LDL) modification, and inflammation is not fully understood.
Purpose of the Study:
- To investigate how different types of shear stress (pulsatile vs. oscillating) affect reactive species production, LDL modification, and inflammatory responses in endothelial cells.
Main Methods:
- Bovine aortic endothelial cells (BAECs) were exposed to pulsatile flow (25 dyne/cm2) or oscillating flow (0 dyne/cm2) with native LDL.
- High-performance liquid chromatography analyzed electronegative LDL species (LDL-, LDL2-).
- NADPH oxidase subunit (gp91phox, Nox4) mRNA expression and monocyte chemoattractant protein-1 (MCP-1) were quantified.
Main Results:
- Oscillating flow upregulated gp91phox and Nox4 mRNA, increasing superoxide production and LDL modification (LDL-, LDL2-).
- Oscillating flow also increased MCP-1 expression and monocyte/BAEC binding.
- Pulsatile flow downregulated gp91phox and Nox4, reduced superoxide and LDL modification, and decreased monocyte/BAEC binding.
Conclusions:
- Flow-dependent LDL oxidation is partly regulated by NADPH oxidase activity.
- Modified LDL formation via superoxide production influences MCP-1 expression and monocyte adhesion.
- Shear stress patterns critically determine endothelial inflammatory responses through modulation of reactive species and LDL modification.