ABSTRACT
The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelialmesenchymal transition (EndMT) induced by transforming growth factor beta (TGFß), was investigated. Human cardiac microvascular endothelial cells were transfected with LVLINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively. The cells were then exposed to TGFß in serumfree medium for 48 h to induce EndMT. Flow cytometric analysis, Cell Counting Kit8 assay and immunofluorescence staining were performed to examine the cell apoptosis rate, assess cell viability, and identify CD31+/αSMA+ doublepositive cells, respectively. Western blotting and reverse transcription quantitative polymerase chain reaction were used to evaluate protein and mRNA expression, respectively. Injury to endothelial cells and EndMT was induced by TGFß in a timedependent manner. LINC00961 overexpression promoted injury and EndMT, whereas LINC00961 knockdown had the opposite effects. Knockdown of LINC00961 attenuated EndMT and injury to endothelial cells induced by TGFß via the PTENPI3KAKT pathway. Inhibition of LINC00961 expression may prevent the occurrence of EndMTrelated cardiovascular diseases, such as myocardial fibrosis and heart failure. Therefore, LINC00961 shows potential as a therapeutic target for cardiovascular diseases.
Subject(s)
Cardiovascular Diseases , RNA, Long Noncoding , Cardiovascular Diseases/metabolism , Endothelial Cells/metabolism , Humans , PTEN Phosphohydrolase/genetics , PTEN Phosphohydrolase/metabolism , Peptides , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Transforming Growth Factor beta/genetics , Transforming Growth Factor beta/metabolismABSTRACT
Objective :To explore influence of sodium creatine phosphate (CP) on percutaneous coronary intervention (PCI)-related myocardial injury in patients with unstable angina pectoris (UAP).Methods : A total of 90 UAP pa-tients ,who were supposed to receive selective PCI ,were selected ,randomly and equally divided into routine treat-ment group and CP group (received CP treatment based on routine medication ).Plasma level of cardiac troponin I (cTnI) before and 18h after PCI ,plasma levels of C reactive protein (CRP) and brain natriuretic peptide (BNP) be- fore and 24h after PCI ,LVEDd ,LVESd and LVEF on two weeks after PCI ,and incidence of major adverse cardio-vascular events (MACE) within two weeks after PCI were measured and compared between two groups .Results :Compared with before PCI ,there was significant rise in plasma cTnI level on 18h after PCI ,and significant reduc-tions in plasma CRP and BNP levels on 24h after PCI in two groups ,P＝0-001 all ;compared with routine treatment group after PCI ,there were significant reductions in plasma levels of cTnI [ (1-58 ± 1-59) mg／L vs.(0-07 ± 0-04) mg／L] ,CRP [ (22-02 ± 2-14) ng／L vs .(11-40 ± 1-49) ng／L] and BNP [ (349-20 ± 28-57) ng／L vs .(175-20 ± 28-55) ng／L] in CP group , P＝0-001 all.Compared with routine treatment group ,there were significant reduc-tions in LVEDd [ (54-83 ± 1-23) mm vs.(50-74 ± 0-97) mm] and LVESd [ (45-65 ± 1-64) mm vs .(42-01 ± 1-84) mm] ,and significant rise in LVEF [ (52-41 ± 1-57)% vs.(65-21 ± 3-36)%] in CP group on two weeks af-ter PCI , P＝0-001 all.On two weeks after PCI ,incidence rate of MACE in CP group was significantly lower than that of routine treatment group (4-44% vs.28-89%) , P＝0-021- Conclusion : CP can significantly reduce plasma levels of cTnI ,CRP and BNP after PCI ,reduce PCI-related myocardial injury .
