Abstract:
:Cardiotrophin-1 (CT-1) can induce expression of the protective heat shock proteins (hsps) in cardiac cells. We show here that, unlike the stress induced accumulation of hsps, the effect of CT-1 is not accompanied by increased hsp mRNA levels and is insensitive to the RNA synthesis inhibitor actinomycin D, suggesting that it occurs at the post-transcriptional level. Pre-treatment with CT-1 reduces the ability of heat shock to induce hsp expression and this effect occurs at the transcriptional level. Hence, CT-1 and stress induce the hsps via different pathways which can antagonise one another. The mechanisms of these effects and their potential impact on the use of CT-1 as a cardioprotective agent are discussed.
journal_name
Cytokinejournal_title
Cytokineauthors
Railson J,Lawrence K,Stephanou A,Brar B,Pennica D,Latchman Ddoi
10.1006/cyto.2000.0778keywords:
subject
Has Abstractpub_date
2000-11-01 00:00:00pages
1741-4issue
11eissn
1043-4666issn
1096-0023pii
S1043-4666(00)90778-6journal_volume
12pub_type
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