M1 macrophage-derived exosomes inhibit cardiomyocyte proliferation through delivering miR-155 - He, Xiaoqing; Liu, Shan; Zhang, Zhanyu; Liu, Qirui; Dong, Juan; Lin, Zhifeng; Chen, Junhao; Li, Lihuan; Liu, Weihua; Liu, Shaojun; Liu, Shiming (BMC cardiovascular disorders, 2024)
Keywords: Analysis; Animals; Antibodies; Cardiomyocyte proliferation; Cardiomyocytes; Care and treatment; Cell Proliferation - drug effects; Cells, Cultured; Coculture Techniques; Diagnosis; Disease Models, Animal; Exosomes; Exosomes - genetics; Exosomes - metabolism; Exosomes - transplantation; Granulocyte-macrophage colony-stimulating factor; Heart; Heart attack; Heart cells; Heart failure; Immunoblotting; Immunofluorescence; Interleukin 6; Interleukin 6 receptors; Interleukin-6 - metabolism; Interleukins; Janus kinase; Janus kinase 2; Janus Kinase 2 - metabolism; Laboratory animals; M1 macrophage; Macrophages; Macrophages - metabolism; Male; Mice, Inbred C57BL; MicroRNA; MicroRNAs - genetics; MicroRNAs - metabolism; Mir-155; miRNA; Myocardial infarction; Myocardial Infarction - genetics; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Penicillin; Phosphorylation; Rats, Sprague-Dawley; Receptors, Interleukin-6 - genetics; Receptors, Interleukin-6 - metabolism; Regeneration; Reporter gene; Risk factors; Signal Transduction; Stat3 protein; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism; γ-Interferon; China; Cardiomyocyte proliferation; Myocardial infarction; Mir-155; Exosomes; M1 macrophage