title: A Natural Model of Mouse Cardiac Myocyte Senescence.
abstract: Many cardiac aging studies are performed on mice first and then, due to difficulty in mouse cardiomyocyte culture, applied the rat neonatal cardiomyocytes to further determine the mechanisms in vitro. Now, the technological challenge of mouse cardiomyocyte culture has been overcome and there is an increasing need for the senescence models of mouse cardiomyocytes. In this study, we have demonstrated that the senescence of mouse cardiomyocytes occurred with the extended culture time as shown by the increased β-galactosidase staining, increased p53 expression, decreased telomere activity, shorted telomere length, increased production of ROS, increased cell apoptosis, and impaired mitochondrial ΔΨm. These senescent responses shared similar results in aged mouse heart tissues in vivo. In summary, we have established and characterized a novel senescence model of mouse cardiomyocytes induced by the extended culture time in vitro. The cell model could be useful for the increased cardiac aging studies worldwide.
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Zunzhe
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Children's Heart Center, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
authors.forename: Xing
authors.initials: X
authors.lastname: Rong
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Bihui
authors.initials: B
authors.lastname: Luo
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Shanshan
authors.initials: S
authors.lastname: Qin
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Lili
authors.initials: L
authors.lastname: Lu
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Xiuli
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Yeying
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA.
authors.forename: Qin
authors.initials: Q
authors.lastname: Hu
authors.affiliation: Department of Pharmacology and Rush University Cardiovascular Research Center, Rush University Medical Center, Chicago, IL, 60612, USA. Zhangchx999@163.com.|Children's Heart Center, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. Zhangchx999@163.com.|Department of Pharmacology, Rush Medical College, Rush University, 1735 West Harrison St, Cohn Building, Suite 406, Chicago, IL, 60612, USA. Zhangchx999@163.com.
authors.forename: Chunxiang
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis; D002478:Cells, Cultured; D016922:Cellular Senescence; D053078:Membrane Potential, Mitochondrial; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D010641:Phenotype; D017382:Reactive Oxygen Species / Q000378:metabolism; D016615:Telomere / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D001616:beta-Galactosidase
keywords: Cardiac aging; Cardiomyocyte; Cell model; Mouse; Senescence