Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2.

Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.

RATIONALE Endothelial cells (EC) at regions exposed to disturbed flow (d-flow) are predisposed to inflammation and the subsequent development of atherosclerosis. We previously showed that thioredoxin interacting protein (TXNIP) was required for tumor necrosis factor-mediated expression of vascular cell adhesion molecule-1. OBJECTIVE We sought to investigate the role of TXNIP in d-flow-induced...

Cellular Biology Thioredoxin Interacting Protein Promotes Endothelial Cell Inflammation in Response to Disturbed Flow by Increasing Leukocyte Adhesion and Repressing Kruppel-Like Factor 2

Novel mechanisms of endothelial mechanotransduction.

Atherosclerosis is a focal disease that develops preferentially where nonlaminar, disturbed blood flow occurs, such as branches, bifurcations, and curvatures of large arteries. Endothelial cells sense and respond differently to disturbed flow compared with steady laminar flow. Disturbed flow that occurs in so-called atheroprone areas activates proinflammatory and apoptotic signaling, and this r...

Sports or statins for atheroprotection? New insight from Kruppel-like factor 2.

Nitric oxide (NO) plays a central role in the control of vascular homeostasis. Adequate NO production stimulated by continuous laminar flow on the endothelial surface, so-called shear stress, prevents endothelial inflammation and development of endothelial dysfunction. Recently, a novel class of mechanosensitive transcription factors has been identified that in endothelial cells transfer shear ...

Kruppel-like factor 2 as a novel mediator of statin effects in endothelial cells.

BACKGROUND Although 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are known to modulate endothelial function, the transcriptional mechanisms underlying these effects are incompletely understood. We hypothesized that Lung-Kruppel-like factor (LKLF/KLF2), a novel and potent regulator of endothelial gene expression, may mediate the downstream effects of statins. Here we repo...