Long non‑coding RNA HIF1A‑AS1 is upregulated in intracranial aneurysms and participates in the regulation of proliferation of vascular smooth muscle cells by upregulating TGF‑β1
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- Published online on: December 28, 2018 https://doi.org/10.3892/etm.2018.7144
- Pages: 1797-1801
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Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Long non-coding (lnc)RNA hypoxia inducible factor 1α-antisense RNA 1 (HIF1A-AS1) not only participates in different types of malignancies, but also serves pivotal roles in thoracic aortic aneurysms, which suggests its possible involvement in intracranial aneurysms. Therefore, the present study aimed to investigate its involvement in intracranial aneurysms. Expression levels of HIF1A‑AS1 and transforming growth factor (TGF)‑β1 in the blood of patients with intracranial aneurysms and healthy controls were detected using reverse transcription‑quantitative polymerase chain reaction. The diagnostic value of blood HIF1A‑AS1 for intracranial aneurysms was analyzed using receiver operating characteristic curve analysis. A HIF1A‑AS1 expression vector was constructed and transfected into human vascular smooth muscle cells (VSMCs) and the effects on cell proliferation and TGF‑β1 expression were explored using the Cell Counting kit‑8 assay and western blot analysis, respectively. Upregulated HIF1A‑AS1 expression levels in blood were observed in patients with intracranial aneurysms when compared with controls. Notably, upregulated HIF1A‑AS1 expression effectively distinguished patients with intracranial aneurysms from healthy controls. Furthermore, HIF1A‑AS1 and TGF‑β1 expression levels were positively correlated with intracranial aneurysms. HIF1A‑AS1 overexpression also upregulated TGF‑β1 expression and inhibited VSMC proliferation. Although TGF‑β1 treatment had no significant effect on HIF1A‑AS1 expression, TGF‑β inhibitor significantly reduced the effects of HIF1A‑AS1 overexpression on cell proliferation. It was therefore concluded that HIF1A‑AS1 may participate in intracranial aneurysms by regulating VSMC proliferation through the upregulation of TGF‑β1.
