The proliferation and migration of vascular smooth muscle cells (VSMCs) are major cellular events in hypertension-induced vascular remodeling, which is closely involved in the progression of atherosclerosis (AS). Although long non-coding RNAs (lncRNAs) are gaining recognition as novel regulators of VSMCs, their functioning and role in AS remain to be elucidated. In the present study, the role of lncRNA ENST00000430945 (lncRNA 430945) in AS was investigated. VSMCs transfected with a small interfering RNA (siRNA; si-430945) and a negative control (si-NC) were used. Cell Counting Kit-8, wound-healing and Transwell migration arrays were performed to determine whether lncRNA 430945 influenced VSMC proliferation and migration. Furthermore, the study examined whether a correlation exists between lncRNA 430945 and the receptor tyrosine kinase-like orphan receptor 2 (ROR2) signaling pathway. It was found that the expression of lncRNA 430945 was high in human AS tissues, which in turn promoted angiotensin II (AngII)-induced VSMC proliferation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analyses showed that lncRNA 430945 mediated the AngII-induced upregulation of ROR2. In addition, the microarray and RT-qPCR results showed that the expression of lncRNA 430945 was increased considerably in AS tissues. The downregulation of lncRNA 430945 significantly suppressed AngII-induced VSMC proliferation and migration. In addition, ROR2 levels in VSMCs transfected with si-430945 were markedly lower than those cells transfected with si-NC. Additionally, western blotting showed that lncRNA 430945 activated the signaling pathways associated with ROR2 and Ras homolog gene family member A (RhoA). The upregulation of lncRNA 430945 in AS promoted the proliferation and migration of VSMCs via activation of the ROR2/RhoA signaling pathway. Therefore, targeting ROR2 or RhoA may be a promising technique in developing therapeutic strategies for treating AS.
The association between inflammatory factor expression and blood pressure with urinary protein in the placenta of pregnant women with pregnancy-induced hypertension (PIH) was investigated to provide a new vision for the clinical prevention and treatment of PIH. Rats were used as animal models and were randomly divided into three groups (control, hypertension and treatment groups) on day 15 of pregnancy with 20 rats in each group. The 10% hypoxia-induced PIH group was induced with administration of an anti-hypertensive drug, and the treatment group was giventreprostinil for one week after the 10% hypoxia-induced PIH. On the 21st day, the experiment was terminated and the placenta was taken to measure the mRNA and protein expression levels of IL-6 and TNF-α, respectively. Pearson's correlation analysis demonstrated the correlation between IL-6 and TNF-α with blood pressure and urinary protein. The blood pressure and urinary protein concentrations in the hypertension group were significantly higher than that in the control group, and the expression levels of IL-6 and TNF-α in the hypertension group were significantly higher (P<0.05). The treatment group significantly reduced inflammatory cytokines and blood pressure and urinary protein levels (P<0.05). Pearson's correlation analysis showed that IL-6 and TNF-α were positively correlated with blood pressure and urinary protein concentration. The blood pressure and urinary protein concentration in PIH rats and the expression levels of IL-6 and TNF-α were significantly higher, and IL-6 and TNF-α were positively correlated with blood pressure and urine protein concentration.
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