Home Bratislava Medical Journal 2016 Bratislava Medical Journal Vol.117, No.7, p.376-380, 2016

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Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.564


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Bratislava Medical Journal Vol.117, No.7, p.376-380, 2016

Title: The role of miR-146a on NF-κB expression level in human umbilical vein endothelial cells under hyperglycemic condition
Author: K. Kamali, E. Salmani Korjan, E. Eftekhar, K. Malekzadeh, F. Ghadiri Soufi

Abstract: Emerging studies have been shown that the expression of micrRNA-146a (miR-146a, as a regulator of nuclear factor κB (NF-κB)), is changed in diabetic patients and animals. This study was designed to evaluate the possible role of miR-146a in the pathogenesis of diabetes-related microvascular complications.
Concurrent with the creation of cellular hyperglycemia (25 mmol/L for 24 h), human umbilical vein endothelial cells (HUVECs) were transfected with 20 nmol/L of hsa-miR-146a antagomir or scramble using HiPerFect reagent (Qiagen). D-mannitol was used as osmotic control.
Hyperglycemia increased the NF-κB gene expression and protein activity (as an inflammation index) in cultured HUVECs. Moreover, the gene expression level of miR-146a, and its target proteins, tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were increased under hyperglycemic condition. The knockdown of miR-146a by transfection of miR-146a antagomir notably increased the NF-κB activity and decreased the NF-κB mRNA in hyperglycemic HUVECs. Furthermore, miR-146a antagomir significantly increased IRAK1 and TRAF6 mRNA levels under hyperglycemic condition.
These results demonstrate that the expression of miR-146a is upregulated in HUVECs during early phase of hyperglycemic condition possibly to regulate the NF-κB activity through inhibition of IRAK1 and TRAF6 (Fig. 4, Ref. 32).

Keywords: hyperglycemia, HUVECs, miRNA-146a, NF-κB, IRAK1, TRAF6
Published online: 12-Jul-2016
Year: 2016, Volume: 117, Issue: 7 Page From: 376, Page To: 380

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