Long noncoding RNAs (lncRNAs) have been found to play important roles in nearly all biological processes. However, the functions of the majority of LncRNAs are not fully clear. Here we evaluated the function of lncRNA OGFRP1, which has not been previously annotated, in human coronary artery endothelial cells (HCAECs). First, we knocked down lncRNA OGFRP1 in HCAECs by using siRNA transfection. qRT-PCR results indicated that siRNA1 and siRNA3 both had potent interference efficiencies. Next, by using CCK8 assay and clone formation assay, we found that siRNA3 transfection induced growth inhibition in HCAECs. Cell migration and invasion were also found to be inhibited in OGFRP1 silenced cells. Moreover, siRNA1 transfection further verified the inhibitory effects of lncRNA OGFRP1 knockdown on the proliferation, migration and invasion of HCAECs. Flow cytometry detection demonstrated that OGFRP1 knockdown induced cell cycle arrest and apoptosis. Western blot assay indicated that p70S6K and CyclinD1 were down-regulated by knockdown of OGFRP1. The intrinsic apoptosis pathway was activated in lncRNA OGFRP1 silenced cells, including increased Bax and Active-caspase 3 and decreased Bcl2. The expression of autophagy markers LC3 and Beclin1 was increased and p62 decreased, all of which indicated that cell autophagy was promoted by down-regulation of lncRNA OGFRP1. Mechanistic studies showed that lncRNA OGFRP1 inhibited the AKT/mTOR signaling pathway, including increasing phosphorylation level of AKT, mTOR and GSK3b. In conclusion, we find that down-regulation of lncRNA induces autophagy and inhibited the proliferation, migration and invasion by AKT/mTOR signaling pathway in HCAECs.

Nucleotide-binding oligomerization domain (NOD)-like receptor proteins (NLRPs) are a subfamily of NOD-like receptors (NLRs) that mainly participate in innate immunity. Among the 14 NLRPs, studies on NLRP2 are few and mostly focus on its functions in reproduction and embryonic development. To the best of the authors' knowledge, there has been no research on the function of NLRP2 in human umbilical vein endothelial cells (HUVECs). The present study knockdown the expression of NLRP2 by transfecting a short interfering (si)RNA (siNLRP2) into HUVECs and investigating its effects on HUVECs. It was identified using a Cell Counting kit-8 assay that knockdown of NLRP2 can inhibit cell proliferation in HUVECs. The results of wound healing and Transwell assays indicated that migration and invasion were also suppressed by siNLRP2 transfection in HUVECs. Flow cytometry demonstrated that siNLRP2 induced cell cycle arrest and apoptosis in HUVECs. Western blot analysis revealed that the expression levels of cell cycle and apoptosis-associated proteins were markedly changed. In addition, knockdown of NLRP2 inhibited the mitogen-activated protein kinase (MAPK) signaling pathway by elevating extracellular signal-regulated kinase phosphorylation levels and reducing proto-oncogene serine/threonine-protein kinase expression. Taken together, it was concluded that NLRP2 served an important role in maintaining cell viability, proliferation and motility in HUVECs, mainly by promoting the MAPK signaling pathway.

In total, 97 acute ST-segment elevation myocardial infarction (STEMI) patients who received an emergency percutaneous coronary intervention (PCI) were enrolled and divided into a ticagrelor group and a clopidogrel group. Thrombolysis in myocardial infarction (TIMI) blood flow and the corrected TIMI frame count (CTFC) were used to assess the blood perfusion of culprit vessels. Thromboelastography (TEG) was used to evaluate the antiplatelet effect of drugs. The results showed that the incidence of TIMI grade III blood flow in the ticagrelor group was significantly higher than that in the clopidogrel group. The CTFC in the anterior descending, circumflex, and right coronary arteries was statistically significantly lower in the ticagrelor group as compared with that in the clopidogrel group. At 2 h and 7 d postdrug treatment, the adenosine diphosphate-induced platelet inhibition rate (ADP%) in the ticagrelor group increased significantly as compared with that in the clopidogrel group, and the platelet aggregation rate of the ADP pathway (MAADP) decreased significantly in the ticagrelor group versus that in the clopidogrel group. In conclusion, ticagrelor significantly improved TIMI blood flow and had a better antiplatelet effect than clopidogrel in STEMI patients undergoing an emergency PCI.