Cardiotrophin-1 induces heat shock protein accumulation in cultured cardiac cells and protects them from stressful stimuli.
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 trypan blue exclusion and LDH release, and by measures of apoptosis, such as propidium-iodide-staining and TUNEL-labelling. Hence, CT-1 can induce the protective hsps and protect cardiac cells from diverse stresses.
Stephanou
A
A
Department of Molecular Pathology, Windeyer Institute of Medical Sciences, University College London Medical School, UK.
Brar
B
B
Heads
R
R
Knight
R D
RD
Marber
M S
MS
Pennica
D
D
Latchman
D S
DS
D000818:Animals; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D016207:Cytokines; D018840:HSP70 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; C092073:cardiotrophin 1