Biomaterial Database

Inhibition of microRNA-346 inhibits myocardial inflammation and apoptosis after myocardial infarction via targeting NFIB. 2020

B Yang, and R Dong, and H Zhao

Department of Cardiology, Chinese PLA General Hospital, Beijing, China. quzhao19990819@163.com.

Acute myocardial infarction (AMI) is a sudden cardiovascular event that endangers human life. MicroRNA is considered to be an important participant in the pathophysiology of myocardial infarction (MI). This article aim was to study the function and mechanisms of microRNA-346 (miR-346) on myocardium after MI. To study the role of miR-346 in MI, we established H2O2-induced H9c2 cell injury model and rat MI model. Real-time polymerase chain reaction (RT-PCR) was used to detect miR-346 expression. Western blot was utilized to measure the expression of Bcl-2, Bax, TNF-α, IL-6 and NFIB. Apoptosis of H9c2 cells was detected by TUNEL staining and flow cytometry. Enzyme-linked immunosorbent assay (ELISA) assay was utilized to measure the levels of TNF-α and IL-6 in supernatant. Assessment of left ventricular function in rats was performed using echocardiography. MiR-346 was significantly upregulated in H2O2-treated H9c2 cells and ischemic myocardium. In the H9c2 cell injury model, the expressions of Bax, TNF-α, and IL-6 were greatly increased while Bcl-2 expression was decreased, and the number of TUNEL-positive cells and apoptosis rate were also significantly increased. At the same time, the levels of TNF-α and IL-6 in the cell supernatant were markedly increased. However, after miR-346 expression was suppressed, these results were reversed. The expression of Bcl-2 increased, while the expression of Bax, TNF-α, and IL-6 decreased. The contents of TNF-α and IL-6 in the cell supernatant also decreased significantly. Both the number of TUNEL-positive cells and the apoptosis rate were markedly reduced. After injecting antagomir-346 into the myocardium of rats to silence miR-346, the cardiac function of MI rats was remarkably improved, and the LDH content in the serum of rats also decreased significantly. Using computational predictions tools, Western blotting and Luciferase activity assay, we found that nuclear factor I/B (NFIB) was targeted by miR-346. The expression of miR-346 was increased in H9c2 cells and ischemic myocardium of MI rats. Silencing miR-346 can significantly inhibit the inflammatory response and the apoptosis of cardiomyocytes by targeting NFIB.

UI	MeSH Term	Description	Entries
D007249	Inflammation	A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.	Innate Inflammatory Response,Inflammations,Inflammatory Response, Innate,Innate Inflammatory Responses
D009203	Myocardial Infarction	NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).	Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D009205	Myocarditis	Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.	Carditis,Myocarditides
D002478	Cells, Cultured	Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.	Cultured Cells,Cell, Cultured,Cultured Cell
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D017207	Rats, Sprague-Dawley	A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.	Holtzman Rat,Rats, Holtzman,Sprague-Dawley Rat,Rats, Sprague Dawley,Holtzman Rats,Rat, Holtzman,Rat, Sprague-Dawley,Sprague Dawley Rat,Sprague Dawley Rats,Sprague-Dawley Rats
D017209	Apoptosis	A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.	Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D051381	Rats	The common name for the genus Rattus.	Rattus,Rats, Laboratory,Rats, Norway,Rattus norvegicus,Laboratory Rat,Laboratory Rats,Norway Rat,Norway Rats,Rat,Rat, Laboratory,Rat, Norway,norvegicus, Rattus
D051839	NFI Transcription Factors	Transcription factors that were originally identified as site-specific DNA-binding proteins essential for DNA REPLICATION by ADENOVIRUSES. They play important roles in MAMMARY GLAND function and development.	CAAT Box Transcription Factor,Nuclear Factor I,Nuclear Factor I-A,Nuclear Factor I-B,Nuclear Factor I-C,Nuclear Factor I-X,Nuclear Factor-1,TGGCA-Binding Protein,Nuclear Factor 1,Nuclear Factor I A,Nuclear Factor I B,Nuclear Factor I C,Nuclear Factor I X,TGGCA Binding Protein,Transcription Factors, NFI
D032383	Myocytes, Cardiac	Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).	Cardiomyocytes,Muscle Cells, Cardiac,Muscle Cells, Heart,Cardiac Muscle Cell,Cardiac Muscle Cells,Cardiac Myocyte,Cardiac Myocytes,Cardiomyocyte,Cell, Cardiac Muscle,Cell, Heart Muscle,Cells, Cardiac Muscle,Cells, Heart Muscle,Heart Muscle Cell,Heart Muscle Cells,Muscle Cell, Cardiac,Muscle Cell, Heart,Myocyte, Cardiac