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

Abstract

These data demonstrate the essential role for TXNIP in mediating EC-leukocyte adhesion under d-flow, as well as define a novel mechanism by which TXNIP acts as a transcriptional corepressor to regulate Kruppel-like factor 2-dependent gene expression.

Full Text

• DOI - Circulation research (DOI)
• Swets Information Services - full-text online
• Ovid Technologies, Inc. - full-text online
• Lippincott Williams & Wilkins - full-text online
• HighWire Press - full-text online

Subjects

• Animals
• Apolipoproteins E
• Atherosclerosis
• Carrier Proteins
• Cells, Cultured
• Coculture Techniques
• Disease Models, Animal
• Down-Regulation
• Endothelial Cells
• Human Umbilical Vein Endothelial Cells
• Humans
• Inflammation
• Kruppel-Like Transcription Factors
• Leukocyte Rolling
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Promoter Regions, Genetic
• RNA Interference
• Regional Blood Flow
• Stress, Mechanical
• Thioredoxins
• Transfection
• Tumor Necrosis Factor-alpha
• Vascular Cell Adhesion Molecule-1

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Authors

• Xiao-Qun Wang
• Patrizia Nigro
• Cameron World
• Keigi Fujiwara
• Chen Yan
• Bradford C Berk

Publication date

2012-02-20

Journal

Journal topics

• Cardiovascular System

Language

Eng.

Copyright

Circulation research

Aab Cardiovascular Research Institute, 601 Elmwood Avenue, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.

Release reference

Circ Res. 2012 Feb;110(4):560-8

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