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

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microRNA-221 regulates high glucose-induced endothelial dysfunction

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

DOI 10.1016/j.bbrc.2009.02.013PMC PMC2670889

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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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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
ORCID: Li, Yangxin
Li, Fan
Lu, Yao Wei
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)
DOI: 10.1016/j.bbrc.2009.02.013
PMC: PMC2670889
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: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
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 (medical) › 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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microRNA-221 regulates high glucose-induced endothelial dysfunction

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