Cardiotrophin-1 reduces stress-induced heat shock protein production in cardiac myocytes.

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

Cytokine

journal_title

Cytokine

authors

Railson J,Lawrence K,Stephanou A,Brar B,Pennica D,Latchman D

doi

10.1006/cyto.2000.0778

keywords:

subject

Has Abstract

pub_date

2000-11-01 00:00:00

pages

1741-4

issue

11

eissn

1043-4666

issn

1096-0023

pii

S1043-4666(00)90778-6

journal_volume

12

pub_type

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