Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice.

Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Research Abstract Details 

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Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Abstract Text:

Li Liu,Xiaojin Zhang,Bo Qian,Xiaoyan Min,Xiang Gao,Chuanfu Li,Yunlin Cheng,Jun Huang,

BACKGROUND: Oxidative stress and myocyte apoptosis are thought to play an important role in the pathogenesis, progression and prognosis of heart failure (HF). Heat shock protein 27 (Hsp27) has been found to confer resistance to oxidative stress in cultured cells; however, the role of Hsp27 in in-vivo hearts remains to be determined. AIM: To investigate the effects of Hsp27 over-expression on doxorubicin-induced HF. METHODS AND RESULTS: Transgenic mice (TG) with cardiac specific over-expression of Hsp27 and their wild type littermates (WT) were challenged with doxorubicin (25 mg/kg, IP) to induce HF. At day 5, TG mice had significantly improved cardiac function and viability and decreased loss of heart weight following doxorubicin exposure compared with WT. In another parallel experiment, doxorubicin-induced increased levels of reactive oxygen species, protein carbonylation, apoptosis and morphologic changes were detected in the mitochondria in WT hearts, whereas these effects were markedly attenuated in TG hearts. In addition, upregulation of heat shock protein 70 and heme oxygenase-1 was present in the TG hearts after doxorubicin stimulation in comparison to WT hearts. CONCLUSION: These findings indicate that Hsp27 may play a key role in resistance to doxorubicin-induced cardiac dysfunction.

Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Publishing Authors By Initials

L Liu,X Zhang,B Qian,X Min,X Gao,C Li,Y Cheng,J Huang,

For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: European journal of heart failure : journal of the

VOLUME: 9

Page Numbers: 762-9

Journal Abbreviation: Eur. J. Heart Fail.

ISSN: 1388-9842

DAY: 4

MONTH: 05

YEAR: 2007

Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Information

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LANGUAGE: eng

NlmUniqueID: 100887595

Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Keywords Mesh Terms:

KEYWORDS: Reactive Oxygen Species

MESH TERMS: analysis

Chemical & Substance for Abstract: Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice. Information

Substance Name: Doxorubicin

Registry Number: 23214-92-8

Grant and Affiliation Information for Over-expression of heat shock protein 27 attenuates doxorubicin-induced cardiac dysfunction in mice.

AFFILIATION: Department of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing, China.

Country: Netherlands

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MEDLINETA: Eur J Heart Fail

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