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microRNA-221 regulates high glucose-induced endothelial dysfunction
Open accessAbstract
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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“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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1 retracted
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Sorted by citations
Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I
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Role of microRNAs in diabetes and its cardiovascular complications
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Non-coding RNAs in Cardiac Remodeling and Heart Failure
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MicroRNAs in Vascular and Metabolic Disease
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Metadata
- 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)
- 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
- 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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