Cited by 158MicroRNA in disease regulationNitric Oxide and Endothelin EffectsAngiogenesis and VEGF in Cancer

microRNA-221 regulates high glucose-induced endothelial dysfunction

Open access
Li, Yangxin, Song, Yao-Hua, Li, Fan, Yang, Tong, Lu, Yao Wei, Geng, Yong-Jian·2009·Biochemical and Biophysical Research Communications

Abstract

Persistent hyperglycemia in diabetes causes endothelial cell dysfunction. Exposure to high levels of glucose, which mimics hyperglycemia, induced expression of microRNA 221 (miR-221) but reduced expression of c-kit, the receptor for stem cell factor in human umbilical vein endothelial cells (HUVECs). In addition, high glucose treatment impaired endothelial cell migration. Incubation with the antisense miR-221 oligonucleotide AMO-221 reduced expression of miR-221 and restored c-kit protein expression in HUVECs treated with high levels of glucose. Furthermore, AMO-221 treatment abolished the inhibitory effect of high glucose exposure on HUVECs transmigration. Thus, under hyperglycemic conditions, miR-221 is induced in HUVECs, which consequently triggers inhibition of c-kit and impairment of HUVECs migration. These findings suggest that manipulation of the miR-221-c-kit pathway may offer a novel strategy for treatment of vascular dysfunction in diabetic patients.

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Crossref · 10.1016/j.bbrc.2009.02.013

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  • Hyperglycemia increases the expression of several microRNAs found in the endothelium, including miR-320, miR-221, miR-503, and miR-125b.

    “Hyperglycemia increases the expression of several microRNAs found in the endothelium, including miR-320, miR-221, miR-503, and miR-125b.”

    From The Vasculature in Prediabetes (2018) · cites this paper as [145]

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Authors
Li, Y., Song, Y.-H., Li, F., Yang, T., Lu, Y. W., & Geng, Y.-J.
Affiliations
  • The University of Texas Health Science Center at Houston (US)
  • The University of Texas MD Anderson Cancer Center (US)
  • Jilin University (CN)
Corresponding author
  • Li, Yangxin
  • Geng, Yong-Jian
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2009-03
Volume
381
Issue
1
Pages
81-83
ISSN
0006-291X (ISSN-L)
OpenAlex
W2001295759
Cited by
158
References
19
Citations by year
2026: 2 · 2025: 2 · 2024: 1 · 2023: 6 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 10 · 2018: 11 · 2017: 12 · 2016: 6 · 2015: 12 · 2014: 16 · 2013: 24 · 2012: 14
FWCI
4.35
Type
journal article
Language
en
Open access
Locations
  • Biochemical and Biophysical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Heart Association (0765149Y)
  • Macdonald Stewart Foundation (07RDM008)
  • National Institutes of Health (R01HL69509)
  • U.S. Department of Defense
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Keywords
miR-221, CD117, high glucose, endothelial dysfunction, hyperglycemia, diabetes mellitus, human umbilical vein endothelial cells, endothelial cell migration, stem cell factor, antisense oligonucleotides, vascular dysfunction
MeSH terms
Cell Movement, Cells, Cultured, Endothelium, Vascular, Glucose, Humans, Hyperglycemia, Proto-Oncogene Proteins c-kit, MicroRNAs

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