Classic Studies of Cultured Cardiac Myocyte Hypertrophy: Interview With a Transformer

@article{Glembotski2013ClassicSO,
  title={Classic Studies of Cultured Cardiac Myocyte Hypertrophy: Interview With a Transformer},
  author={Christopher C. Glembotski},
  journal={Circulation Research},
  year={2013},
  volume={113},
  pages={1112–1116}
}
  • C. Glembotski
  • Published 25 October 2013
  • Biology, Medicine
  • Circulation Research
Differentiation of Rat Myocytes in Single Cell Cultures With and Without Proliferating Nonmyocardial Cells Simpson, P. and Savion, S. Circ Res. 1982;50:101–116 Myocyte Hypertrophy in Neonatal Rat Heart Cultures and Its Regulation by Serum and by Catecholamines Simpson, P., McGrath, A., and Savion, S. Circ Res . 1982;51:787–801 Stimulation of Hypertrophy of Cultured Neonatal Rat Heart Cells Through an α1-Adrenergic Receptor and Induction of Beating Through an α1- and β1-Adrenergic… 

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References

SHOWING 1-10 OF 39 REFERENCES

Autonomous and growth factor-induced hypertrophy in cultured neonatal mouse cardiac myocytes. Comparison with rat.

It is concluded that mouse myocytes have a unique autonomous hypertrophy in the absence of added growth factors, with increases in cell area, protein content, and the mRNAs for atrial natriuretic factor and beta-MyHC.

Cardiokines: recent progress in elucidating the cardiac secretome.

The sets of proteins secreted from cells, ie, secretomes, play crucial roles in intercellular and intertissue communication during tissue development and growth and in response to various

Stimulation of hypertrophy of cultured neonatal rat heart cells through an alpha 1-adrenergic receptor and induction of beating through an alpha 1- and beta 1-adrenergic receptor interaction. Evidence for independent regulation of growth and beating.

  • P. Simpson
  • Biology, Medicine
    Circulation research
  • 1985
Analysis of the effect of adrenergic agents on hypertrophy and beating of myocytes in serum-free cultures implies that growth and beating can be regulated independently through separate cellular pathways.

Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response.

  • P. Simpson
  • Biology, Medicine
    The Journal of clinical investigation
  • 1983
Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response, and this response was inhibited by the nonselective alpha adrenergic antagonist phentolamine and by the alpha 2 adrenergic antagonists prazosin and terazosin.

Transgenic Galphaq overexpression induces cardiac contractile failure in mice.

The Galphaq overexpressor exhibits a biochemical and physiologic phenotype resembling both the compensated and decompensated phases of human cardiac hypertrophy and suggests a common mechanism for their pathogenesis.

Transgenic Gαq overexpression induces cardiac contractile failure in mice

The Gαq overexpressor exhibits a biochemical and physiologic phenotype resembling both the compensated and decompensated phases of human cardiac hypertrophy and suggests a common mechanism for their pathogenesis.

&bgr;-Myosin Heavy Chain Is Induced by Pressure Overload in a Minor Subpopulation of Smaller Mouse Cardiac Myocytes

The data challenge the current paradigm of the fetal hypertrophic gene program and identify a new subpopulation of smaller working ventricular myocytes with more myosin in a minor sub population of smaller cardiac myocytes.

Decompensation of Pressure-Overload Hypertrophy in Gαq-Overexpressing Mice

The effects of intrinsic myocyte Gαq signaling on the left ventricular hypertrophic response to experimental pressure overload, and a pattern of fetal gene expression similar to the known characteristics of nontransgenic pressure-overloaded mice are determined.

Signaling mechanisms for the activation of an embryonic gene program during the hypertrophy of cardiac ventricular muscle.

  • R. Chien
  • Biology
    Basic research in cardiology
  • 1992
Co-transfection of a dominant negative RAS vector effectively inhibits the induction of the ANF gene during alpha adrenergic mediated hypertrophy of ventricular muscle cells, thereby establishing that a RAS-mediated pathway is required for ANF induction.

Cardiac α1-adrenergic drive in pathological remodelling

In the presence of pressure overload or with myocardial infarction, activation of α1-ARs appears to produce important pro-survival effects at the level of the cardiomyocyte, and to protect against maladaptive cardiac remodelling and decompensation to heart failure.