Proteomic investigation of embryonic rat heart-derived H9c2 cell line sheds new light on the molecular phenotype of the popular cell model.

[1]  F. V. van Nieuwenhoven,et al.  Stable transfection of fatty acid translocase (CD36) in a rat heart muscle cell line (H9c2). , 1998, Journal of lipid research.

[2]  G. Schultz,et al.  Morphological, biochemical, and electrophysiological characterization of a clonal cell (H9c2) line from rat heart. , 1991, Circulation research.

[3]  Differentiation-Dependent Doxorubicin Toxicity on H9c2 Cardiomyoblasts , 2012, Cardiovascular Toxicology.

[4]  M. Štěrba,et al.  Oxidative stress, redox signaling, and metal chelation in anthracycline cardiotoxicity and pharmacological cardioprotection. , 2013, Antioxidants & redox signaling.

[5]  G. V. van Eys,et al.  Smoothelin, a novel cytoskeletal protein specific for smooth muscle cells , 1996, The Journal of cell biology.

[6]  E. Yeh,et al.  Identification of the molecular basis of doxorubicin-induced cardiotoxicity , 2012, Nature Medicine.

[7]  D. Triggle.  L-type calcium channels. , 2006, Current pharmaceutical design.

[8]  R. Ravazzolo,et al.  A DNA element in the alpha1 type III collagen promoter mediates a stimulatory response by angiotensin II. , 2000, Kidney international.

[9]  P. Lyu,et al.  Proteomics study of oxidative stress and Src kinase inhibition in H9C2 cardiomyocytes: A cell model of heart ischemia reperfusion injury and treatment , 2010 .

[10]  F. Ramaekers,et al.  Titin expression as an early indication of heart and skeletal muscle differentiation in vitro. Developmental re-organisation in relation to cytoskeletal constituents , 1996, Journal of Muscle Research & Cell Motility.

[11]  H. Chou,et al.  Hyaluronic acid-dependent protection in H9C2 cardiomyocytes: a cell model of heart ischemia-reperfusion injury and treatment. , 2013, Toxicology.

[12]  Phillip C. Wright,et al.  An insight into iTRAQ: where do we stand now? , 2012, Analytical and Bioanalytical Chemistry.

[13]  B W Kimes,et al.  Properties of a clonal muscle cell line from rat heart. , 1976, Experimental cell research.

[14]  Miss A.O. Penney.  (b) , 1974, The New Yale Book of Quotations.

[15]  B. Binder,et al.  A highly conserved proapoptotic gene, IKIP, located next to the APAF1 gene locus, is regulated by p53 , 2004, Cell Death and Differentiation.

[16]  P. Oliveira,et al.  Metabolic Remodeling During H9c2 Myoblast Differentiation: Relevance for In Vitro Toxicity Studies , 2011, Cardiovascular Toxicology.

[17]  Brendan MacLean,et al.  Bioinformatics Applications Note Gene Expression Skyline: an Open Source Document Editor for Creating and Analyzing Targeted Proteomics Experiments , 2022 .

[18]  P. Oliveira,et al.  Gene Expression Profiling of H9c2 Myoblast Differentiation towards a Cardiac-Like Phenotype , 2015, PloS one.

[19]  P. Oliveira,et al.  Isoproterenol Cytotoxicity is Dependent on the Differentiation State of the Cardiomyoblast H9c2 Cell Line , 2011, Cardiovascular Toxicology.

[20]  Andrew Emili,et al.  Proteome Dynamics during C2C12 Myoblast Differentiation*S , 2005, Molecular & Cellular Proteomics.

[21]  D. Aggarwal,et al.  Analysis of proteome changes in doxorubicin-treated adult rat cardiomyocyte. , 2011, Journal of proteomics.

[22]  G. Tomaselli,et al.  Simultaneous expression of cardiac and skeletal muscle isoforms of the L‐type Ca2+ channel in a rat heart muscle cell line. , 1994, The Journal of physiology.

[23]  B. Hinz,et al.  Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. , 2012, The American journal of pathology.

[24]  M. Štěrba,et al.  Molecular Remodeling of Left and Right Ventricular Myocardium in Chronic Anthracycline Cardiotoxicity and Post-Treatment Follow Up , 2014, PloS one.

[25]  Rajendra K. Sharma,et al.  Cardiomyocyte culture - an update on the in vitro cardiovascular model and future challenges. , 2013, Canadian journal of physiology and pharmacology.

[26]  S. Gygi,et al.  Quantitative analysis of complex protein mixtures using isotope-coded affinity tags , 1999, Nature Biotechnology.

[27]  G. G. Stokes.  "J." , 1890, The New Yale Book of Quotations.

[28]  Elena Bisetto,et al.  Cardiac differentiation promotes mitochondria development and ameliorates oxidative capacity in H9c2 cardiomyoblasts. , 2011, Mitochondrion.

[29]  G. Schuurhuis,et al.  Doxorubicin (adriamycin): a critical review of free radical-dependent mechanisms of cytotoxicity. , 1990, Pharmacology & therapeutics.

[30]  G. Ravenscroft,et al.  Evidence of altered guinea pig ventricular cardiomyocyte protein expression and growth in response to a 5 min in vitro exposure to H(2)O(2). , 2010, Journal of proteome research.

[31]  Gilles Caraux,et al.  PermutMatrix: a graphical environment to arrange gene expression profiles in optimal linear order , 2005, Bioinform..

[32]  L. Marks,et al.  Lung , 2013, ALERT • Adverse Late Effects of Cancer Treatment.

[33]  E. Marbán,et al.  L-type calcium channels, potassium channels, and novel nonspecific cation channels in a clonal muscle cell line derived from embryonic rat ventricle. , 1991, Circulation research.

[34]  L. Leinwand,et al.  Localization of types I, III and IV collagen mRNAs in rat heart cells by in situ hybridization. , 1989, Journal of molecular and cellular cardiology.

[35]  T. Sasaki,et al.  Doxorubicin-induced inhibition of prolyl hydroxylation during collagen biosynthesis in human skin fibroblast cultures. Relevance to imparied wound healing. , 1987, The Journal of clinical investigation.

[36]  O. Issinger,et al.  Comparative analysis of stress responses of H9c2 rat cardiomyoblasts following treatment with doxorubicin and tBOOH. , 2012, Experimental cell research.

[37]  P. Mammen,et al.  Regulation of myoglobin expression , 2010, Journal of Experimental Biology.

[38]  C. Scharf,et al.  Proteomic analysis of doxorubicin‐induced changes in the proteome of HepG2cells combining 2‐D DIGE and LC‐MS/MS approaches , 2010, Proteomics.

[39]  J. Mason,et al.  Anthracycline cardiomyopathy monitored by morphologic changes. , 1978, Cancer treatment reports.

[40]  Xinxin Guo,et al.  Anthracyclines Induce Calpain-dependent Titin Proteolysis and Necrosis in Cardiomyocytes* , 2004, Journal of Biological Chemistry.

[41]  P. Lyu,et al.  Proteomics study of oxidative stress and Src kinase inhibition in H9C2 cardiomyocytes: a cell model of heart ischemia-reperfusion injury and treatment. , 2010, Free radical biology & medicine.

[42]  Y. J. Kang,et al.  Calcineurin Activation Is Not Necessary for Doxorubicin-Induced Hypertrophy in H9c2 Embryonic Rat Cardiac Cells: Involvement of the Phosphoinositide 3-Kinase-Akt Pathway , 2006, Journal of Pharmacology and Experimental Therapeutics.

[43]  Peter Gluchowski,et al.  F , 1934, The Herodotus Encyclopedia.

[44]  M. Pfaffl,et al.  A new mathematical model for relative quantification in real-time RT-PCR. , 2001, Nucleic acids research.

[45]  John B. Shoven,et al.  I , Edinburgh Medical and Surgical Journal.

[46]  R. Woodworth,et al.  Myoglobin Expression in L 6 Muscle Cells , 2022 .

[47]  M. Peckham,et al.  Myogenic cells express multiple myosin isoforms , 1997, Journal of Muscle Research & Cell Motility.

[48]  C. Lim,et al.  Disruption of a GATA4/Ankrd1 Signaling Axis in Cardiomyocytes Leads to Sarcomere Disarray: Implications for Anthracycline Cardiomyopathy , 2012, PloS one.

[49]  Mohit M. Jain,et al.  Isolation, culture, and functional analysis of adult mouse cardiomyocytes. , 2007, Methods in molecular medicine.

[50]  L. Kedes,et al.  Doxorubicin selectively inhibits muscle gene expression in cardiac muscle cells in vivo and in vitro. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[51]  P. Oliveira,et al.  Mitochondrial disruption occurs downstream from β-adrenergic overactivation by isoproterenol in differentiated, but not undifferentiated H9c2 cardiomyoblasts: differential activation of stress and survival pathways. , 2013, The international journal of biochemistry & cell biology.

[52]  Li Li,et al.  The mitochondrial inner membrane protein mitofilin controls cristae morphology. , 2005, Molecular biology of the cell.

[53]  P. Lory,et al.  Modulation of L-type Calcium Channel Expression during Retinoic Acid-induced Differentiation of H9C2 Cardiac Cells* , 1999, The Journal of Biological Chemistry.

[54]  M. Markman,et al.  Expression of the smooth‐muscle proteins α‐smooth‐muscle actin and calponin, and of the intermediate filament protein desmin are parameters of cardiomyocyte maturation in the prenatal rat heart , 1997, The Anatomical record.