Abstract
Thoracic aortic aneurysm (TAA) has been causing the death of elder people. Myosin heavy chain 11 (Myh11) has been reported associated with aortic aneurysm, but there is no specific study on its function on TAA. Here we aimed to explore the function of Myh11 on mouse aortic smooth muscle cells (SMCs) for studying the inner mechanism of TAA. H2O2 treatment was implemented on mouse aortic SMCs for detecting cell apoptosis. Meanwhile, functional assays were conducted to verify the function of Myh11 on mouse aortic SMCs. Also, pull-down assay, RIP assay were implemented to identify the potential RNAs for study. Quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay were implemented to identify the expression and binding relationships of RNAs. Myh11 expression was increased by treatment of H2O2. Myh11 could decrease proliferation and enhance apoptosis of mouse aortic SMCs. At the same time, mmu-miR-330-5p could bind to Myh11 and Sox2ot, forming a competing endogenous RNA (ceRNA) pathway to regulate the proliferation and apoptosis of mouse aortic SMCs. Moreover, both Sox2ot and Myh11 were proved to be up-regulated whereas miR-330-5p down-regulated in Fbn1C1039G/+ mice, the in vivo model of TAA. In a word, long noncoding RNA (lncRNA) Sox2ot modulates the progression of TAA by regulating miR-330-5p/Myh11 axis.
Highlights
Thoracic aortic aneurysm (TAA) has been affecting people’s health and is considered as a serious vascular disease [1]
We studied the expression of Myosin heavy chain 11 (Myh11) in mouse aortic smooth muscle cell (SMC) (MOVAS and A10) at first. Quantitative real-time polymerase chain reaction (qRT-PCR) assay revealed that Myh11 was up-regulated by H2O2 (800 μmol/l) treatment in a time-dependent manner (Figure 1A)
TUNEL assay and flow cytometry analysis showed that increased cell apoptosis caused by H2O2 (800 μmol/l) treatment was significantly decreased again by
Summary
Thoracic aortic aneurysm (TAA) has been affecting people’s health and is considered as a serious vascular disease [1]. TAA mainly occurs after the age of 60, and male patients occupy 80% of TAA cases [2,3]. Most of the TAA cases are caused by the deterioration of atherosclerosis, and a few cases are caused by syphilis [3,4]. Surgical treatment has become the most effective therapy for TAA. The surgical procedure is complicated and has high risk [3,4,5]. Thence, it is of vital importance for us to explore the deeper molecular mechanisms in TAA
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