Tissue factor expression is differentially modulated by cyclic mechanical strain in various human endothelial cells

Area of Science:

• Vascular Biology
• Hemostasis
• Cellular Physiology

Background:

• Endothelial cell (EC) hemostatic properties are influenced by chemical and mechanical factors.
• EC responses vary based on their anatomical origin within the vascular tree.

Purpose of the Study:

• To investigate the effects of cyclic strain, tumor necrosis factor alpha (TNF alpha), or both on tissue factor (TF) activity in human EC from diverse sources.
• To understand the differential modulation of endothelial procoagulant potential by hemodynamic stimuli.

Main Methods:

• Used a chromogenic assay to measure TF activity.
• Exposed human umbilical vein EC (HUVEC), human aortic EC (HAEC), and human microvascular EC (HMVEC) to cyclic strain and/or TNF alpha.
• Investigated the role of cyclic AMP (cAMP) and protein kinase C (PKC) pathways.

Main Results:

• Basal TF activity was low in all EC types.
• TNF alpha increased TF activity diversely across EC types.
• Cyclic strain elevated TF activity in HMVEC and HAEC, but not HUVEC.
• Synergistic TF expression occurred in HMVEC with combined stimuli.
• TNF alpha-induced TF activity involved PKC and cAMP pathways, while cyclic strain acted independently.

Conclusions:

• TNF alpha and cyclic strain differentially modulate TF activity in human EC based on their origin.
• Hemodynamic stimuli have varied effects on the procoagulant potential of different endothelial cells.
• Understanding these differential responses is crucial for vascular hemostasis research.