ArticleJournal of cellular and molecular medicine2019
Long non-coding RNA GAPLINC promotes angiogenesis by regulating miR-211 under hypoxia in human umbilical vein endothelial cells.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- In vitro and in vivo studies of GAPLINC identify it as a critical host factor involved in the regulation of influenza A virus infection.Veterinary research · 2026Article
- LncRNAs Are Key Regulators of Transcription Factor-Mediated Endothelial Stress Responses.International journal of molecular sciences · 2024Review
- lncRNA GAPLINC regulates vascular endothelial cell apoptosis in atherosclerosis.Archives of medical science : AMS · 2024Article
- A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma.Cancer cell international · 2022Article
- LncRNA Snhg1 Plays an Important RoleFrontiers in genetics · 2022Article
- The role of hypoxia-induced long noncoding RNAs (lncRNAs) in tumorigenesis and metastasis.Biomedical journal · 2021Review
- Expression and Clinical Value of LncRNA GAPLINC in Esophageal Squamous Cell Carcinoma.OncoTargets and therapy · 2021Article
- Long non-coding RNA GAPLINC promotes angiogenesis by regulating miR-211 under hypoxia in human umbilical vein endothelial cells.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the role of a long non-coding RNA GAPLINC in angiogenesis using human umbilical vein endothelial cells (HUVEC). We found that hypoxia and hypoxia-inducible factor 1α (HIF-1α) increased the expression of GAPLINC in HUVEC cells. Moreover, GAPLINC overexpression down-regulated miR-211 and up-regulated Bcl2 protein expression. Further rescue experiments confirmed that hypoxia directly increased GAPLINC expression. GAPLINC overexpression also increased cell migration and vessel formation which promoted angiogenesis, and these changes were attributed to the increased expression of vascular endothelial growth factor receptors (VEGFR) and delta-like canonical notch ligand 4 (DLL4) receptors. Finally, we demonstrated that GAPLINC promotes vessel formation and migration by regulating MAPK and NF-kB signalling pathways. Taken together, these findings comprehensively demonstrate that overexpression of GAPLINC increases HUVEC cells angiogenesis under hypoxia condition suggesting that GAPLINC can be a potential target for critical limb ischaemia (CLI) treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.