Cardiotrophin-1 induces heat shock protein accumulation in cultured cardiac cells and protects them from stressful stimuli.

@article{Stephanou1998Cardiotrophin1IH,
  title={Cardiotrophin-1 induces heat shock protein accumulation in cultured cardiac cells and protects them from stressful stimuli.},
  author={Anastasis Stephanou and Bhawanjit K. Brar and Richard John Heads and Richard D Knight and Michael Marber and Diane Pennica and D. S. Latchman},
  journal={Journal of molecular and cellular cardiology},
  year={1998},
  volume={30 4},
  pages={849-55}
}
Cardiotrophin-1 (CT-1) was originally identified as a molecule capable of inducing cardiac hypertrophy. We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90, with hsp70 levels being enhanced three-fold and hsp90 levels being enhanced seven-fold. Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress, as assayed both by measures of total cell death, such as… CONTINUE READING

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Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Heat shock proteinsIs biochemical function of gene productHSP90 Heat-Shock Proteins
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90 , with hsp70 levels being enhanced three - fold and hsp90 levels being enhanced seven - fold .
Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress , as assayed both by measures of total cell death , such as trypan blue exclusion and LDH release , and by measures of apoptosis , such as propidium - iodide - staining and TUNEL - labelling .
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