OBJECTIVE: The aim of this study was to investigate the long non-coding RNA (lncRNA) HULC in promoting angiogenesis after myocardial infarction (MI) and to further investigate its possible mechanism. MATERIALS AND METHODS: Twenty-four male Sprague Dawley (SD) rats were randomly divided into two groups, namely, operation group and control group. The rats in the operation group were induced by ligation of the left anterior descending coronary artery, while those in control group received the same surgery without ligating the blood vessels. Seven days after the operation, the myocardial tissues of rats were collected to detect HULC expression by quantitative real-time polymerase chain reaction (RT-PCR). At the same time, the expression of HULC in primary myocardial cells and cardiac microvascular endothelial cells were induced by hypoxia. A hypoxia model was constructed in HUVEC cells, and the effects of HULC were explored by RT-PCR, Western blot Technology (WB), Cell Counting Kit-8 (CCK8) assay, EdU staining, Tube-like structure formation experiments. Thereafter, HULC downstream miRNAs were verified by Luciferase, pull-down, and RNA IP experiments. Similarly, the effects of miR-29b on HUVEC were verified by RT-PCR, WB, CCK8 assay, EdU staining, and tube-like structure formation experiments, respectively. RESULTS: RT-PCR detection results showed that the expression of HULC in myocardial tissues was down-regulated after MI, and the expression of HULC in cardiac microvascular endothelial cells was decreased under hypoxia-induced inflammation. In addition, the overexpression of HULC in HUVEC cells could inhibit the expressions of inflammatory factors (IL-1, IL-6 and IL-8) and promote angiogenesis (increased cell viability, increased tube-like structure formation, and increased cell proliferation). Through Dual-Luciferase reporter gene experiments, it was found that HULC could directly target miR-29b. At the same time, miR-29 overexpression significantly reversed the effects of HULC on cell viability, pro-inflammatory cytokines, and angiogenesis. CONCLUSIONS: LncRNA HULC protects HUVEC cells from hypoxia-induced inflammation damage by interacting with miR-29b and inhibiting its expression, and it can also promote angiogenesis.
OBJECTIVE: The aim of this study was to investigate the long non-coding RNA (lncRNA) HULC in promoting angiogenesis after myocardial infarction (MI) and to further investigate its possible mechanism. MATERIALS AND METHODS: Twenty-four male Sprague Dawley (SD) rats were randomly divided into two groups, namely, operation group and control group. The rats in the operation group were induced by ligation of the left anterior descending coronary artery, while those in control group received the same surgery without ligating the blood vessels. Seven days after the operation, the myocardial tissues of rats were collected to detect HULC expression by quantitative real-time polymerase chain reaction (RT-PCR). At the same time, the expression of HULC in primary myocardial cells and cardiac microvascular endothelial cells were induced by hypoxia. A hypoxia model was constructed in HUVEC cells, and the effects of HULC were explored by RT-PCR, Western blot Technology (WB), Cell Counting Kit-8 (CCK8) assay, EdU staining, Tube-like structure formation experiments. Thereafter, HULC downstream miRNAs were verified by Luciferase, pull-down, and RNA IP experiments. Similarly, the effects of miR-29b on HUVEC were verified by RT-PCR, WB, CCK8 assay, EdU staining, and tube-like structure formation experiments, respectively. RESULTS: RT-PCR detection results showed that the expression of HULC in myocardial tissues was down-regulated after MI, and the expression of HULC in cardiac microvascular endothelial cells was decreased under hypoxia-induced inflammation. In addition, the overexpression of HULC in HUVEC cells could inhibit the expressions of inflammatory factors (IL-1, IL-6 and IL-8) and promote angiogenesis (increased cell viability, increased tube-like structure formation, and increased cell proliferation). Through Dual-Luciferase reporter gene experiments, it was found that HULC could directly target miR-29b. At the same time, miR-29 overexpression significantly reversed the effects of HULC on cell viability, pro-inflammatory cytokines, and angiogenesis. CONCLUSIONS: LncRNA HULC protects HUVEC cells from hypoxia-induced inflammation damage by interacting with miR-29b and inhibiting its expression, and it can also promote angiogenesis.