RESUMO
ABSTRACT: Myocardial infarction (MI) is a leading cause of heart failure all over the world. Long noncoding RNAs have been reported to be associated with the development of MI. In this article, we aimed to explore the effects of long noncoding RNA small nuclear RNA host gene 7 (SNHG7) on MI and the possible mechanism. In this study, an MI model was established by ligating the left anterior descending coronary artery of mice. Cardiac fibroblasts (CFs) derived from neonatal mice were activated by angiotensin II (Ang-II) treatment. The expression of SNHG7 and miR-455-3p was examined by quantitative real-time polymerase chain reaction, and protein levels of platelet-activating factor receptor (PTAFR) and fibrosis-related proteins were analyzed by western blot assay. Cell apoptosis of CFs was monitored by flow cytometry. Enzyme-linked immunosorbent assay was performed to evaluate inflammatory responses in CFs. Moreover, dual-luciferase reporter assay was used to confirm the target relationship between miR-455-3p and SNHG7 or PTAFR. LncRNA SNHG7 and PTAFR were upregulated, whereas miR-455-3p was downregulated in cardiac tissues of mice with MI and Ang-II-induced CFs. SNHG7 depletion or miR-455-3p overexpression attenuated Ang-II-induced apoptosis, fibrosis, and inflammation in CFs, which was severally weakened by miR-455-3p inhibition or PTAFR upregulation. LncRNA SNHG7 targeted miR-455-3p, and PTAFR was a target of miR-455-3p. LncRNA SNHG7 depletion exerted protective roles in apoptosis, fibrosis, and inflammation in Ang-II-induced CFs by regulating miR-455-3p/PTAFR axis, providing a potential molecular target for MI therapy.
Assuntos
MicroRNAs/genética , Infarto do Miocárdio/genética , Glicoproteínas da Membrana de Plaquetas/genética , RNA Longo não Codificante/genética , Receptores Acoplados a Proteínas G/genética , Animais , Apoptose/genética , Células Cultivadas , Modelos Animais de Doenças , Regulação para Baixo , Fibroblastos/citologia , Fibrose/genética , Técnicas de Silenciamento de Genes , Inflamação/genética , Inflamação/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Infarto do Miocárdio/fisiopatologia , RNA Nuclear Pequeno/genética , Regulação para CimaRESUMO
Transition metal sulfides (TMSs) have been demonstrated as attractive anodes for potassium-ion batteries (KIBs) due to the high capacity, abundant resource, and excellent redox reversibility. Unfortunately, practical implementation of TMSs to KIBs is still hindered by the unsatisfactory cyclability and rate performance which result from the vast volume variation during charge/discharge processes. Herein, a uniform nitrogen-doped carbon coated Cu2S hollow nanocube (Cu2S@NC) is designed as an anode material for the KIB, which displays an outstanding cycle performance (317 mAh g-1 after 1200 cycles at 1 A g-1) and excellent rate capacity (257 mAh g-1 at 6 A g-1) in a half-cell. The hollow nanosized structure can both shorten the diffusion length of potassium ions/electrons and buffer the volume expansion upon cycling. Besides, the high concentration electrolyte is beneficial to form the stable solid electrolyte interphase (SEI) film, reducing the interface impedance and enhancing the cycling stability. Ex situ transmission electron microscopy (TEM) and ex situ X-ray diffraction (XRD) reveal the reaction mechanism of Cu2S@NC.
