BACKGROUND: Preliminary microarray data in our laboratory indicated that the novel long noncoding RNA (lncRNA), GASL1, was downregulated in patients with intracranial aneurysms. This study aimed to investigate the expression of lncRNA GASL1 in patients with intracranial aneurysms and its role in the regulation of vascular smooth muscle cell (VSMC) proliferation by transforming growth factor-β1 (TGF-β1).

MATERIAL AND METHODS: The study included 68 patients with unruptured intracranial aneurysms and 56 healthy volunteers. In both groups, serum levels of TGF-β1 were measured using an enzyme-linked immunoassay (ELISA) and Western blot. Human VSMCs in vitro underwent lncRNA GASL1 overexpression using the insertion of an EcoRI-EcoRI fragment into the pIRSE2 vector. Cell viability and proliferation were measured by a cell counting kit-8 (CCK-8) assay. RNA extraction and quantitative real-time polymerase chain reaction (qRT-PCR) determined GASL1 expression.

RESULTS: ROC curve analysis showed that downregulation of GASL1 effectively distinguished patients with intracranial aneurysm from healthy controls. Blood GASL1 and TGF-β1 were negatively correlated in patients with intracranial aneurysm but not in healthy people. GASL1 overexpression promoted proliferation of human vascular smooth muscle cells (VSMCs) and downregulated TGF-β1 expression, while exogenous TGF-β1 reduced VSMCs proliferation but showed no effects on GASL1 expression. 

CONCLUSIONS: Expression of the novel lncRNA, GASL1, was downregulated in patients with intracranial aneurysms and regulated the proliferation of VSMCs in vitro by targeting TGF-β1.

Keywords: intracranial aneurysm, Muscle, Smooth, Vascular, Case-Control Studies, Down-Regulation, Myocytes, Smooth Muscle, Transforming Growth Factor beta1