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Thioredoxin-interacting protein promotes high-glucose-induced macrovascular endothelial dysfunction.

Abstract：

:Thioredoxin-interacting protein (TXNIP) emerges as a central regulator for glucose homeostasis, which goes awry in diabetic subjects. Endothelial dysfunction is considered the earliest detectable stage of cardiovascular disease (CVD), a major complication of diabetes. Here, we hypothesize that TXNIP may promote endothelial dysfunction seen in Type 1 diabetes mellitus (T1D). Using a T1D-like rat model, we found that diabetic rats showed significantly higher TXNIP mRNA and protein levels in peripheral blood, compared to their non-diabetic counterparts. Those changes were accompanied by decreased production of nitric oxide (NO) and vascular endothelial growth factor (VEGF), concurrent with increased expression of reactive oxygen species (ROS) and vascular cell adhesion molecule 1 (VCAM-1) in the aortic endothelium. In addition, TXNIP overexpression in primary human aortic endothelial cells (HAECs) induced by either high glucose or overexpression of carbohydrate response element binding protein (ChREBP), a major transcriptional activator of TXNIP, promoted early apoptosis and impaired NO bioactivity. The correlation between TXNIP expression levels and endothelial dysfunction suggests that TXNIP may be a potential biomarker for vascular complications in T1D patients.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Li X,Kover KL,Heruth DP,Watkins DJ,Guo Y,Moore WV,He LG,Zang M,Clements MA,Yan Y

doi

10.1016/j.bbrc.2017.09.028

subject

Has Abstract

pub_date

2017-11-04 00:00:00

pages

291-297

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(17)31788-6

journal_volume

493

pub_type

杂志文章

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