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Transgenic overexpression of HSP56 does not result in cardiac hypertrophy nor protect from ischaemia/reperfusion injury

Transgenic overexpression of HSP56 does not result in cardiac hypertrophy nor protect from ischaemia/reperfusion injury
Transgenic overexpression of HSP56 does not result in cardiac hypertrophy nor protect from ischaemia/reperfusion injury
Heat shock proteins are known to be induced during and following different forms of cardiac stress. It has previously been shown that their expression is beneficial for the heart following trauma such as ischaemia–reperfusion (I/R) injury. Heat shock protein 56 (HSP56) belongs to the family of FK506-binding immunophilin proteins and is found in steroid receptor complexes, notably the glucocorticoid receptor. We have previously shown that HSP56 and other HSPs are induced in cardiac myocytes treated with cardiotrophin-1, a cytokine with potent hypertrophic and protective properties on cardiac cells. The hypertrophic action of cardiotrophin-1 on cardiac cells is dependent on HSP56 induction and overexpression of HSP56 is sufficient for inducing hypertrophy in cardiac cells. To investigate this phenomenon in vivo, we have generated transgenic mice overexpressing HSP56 and assessed them for the development cardiac hypertrophy and resistance of their hearts to I/R-injury by Langendorff perfusion. Mice generated demonstrated stable, yet varying expression levels of HSP56. Initial characterisation identified a sex-specific phenotype where male overexpressing mice exhibited a moderate, but significant, reduced body weight compared to wild-type controls. In ex vivo stress analyses we found, unexpectedly, that significant overexpression of HSP56 does not induce myocardial hypertrophy and nor does it protect the intact heart from I/R-injury. These observations now suggest a more intricate HSP56-Sp. Cardiophenotype that requires further studies to determine if HSP56 is necessary in mediating hypertrophy induced by other myocardial stimuli.

1357-2725
74-79
Carroll, Christopher J.
83f87248-a322-4c00-b0e0-a54119376c26
Suleman, Naushaad
235ff49f-d9f5-421f-90f1-25121517fe90
Davidson, Sean M.
b8eeed87-5d86-42ca-8844-25bf6887253c
Faulkes, David J.
deb5b229-ba15-407e-a9a7-f8af69dabf12
Diss, James K.
321de9b3-e7ec-488f-adff-779c8cd9c38f
Knight, Richard
76cd0c41-511b-475a-af63-938b74ef8270
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db
Carroll, Christopher J.
83f87248-a322-4c00-b0e0-a54119376c26
Suleman, Naushaad
235ff49f-d9f5-421f-90f1-25121517fe90
Davidson, Sean M.
b8eeed87-5d86-42ca-8844-25bf6887253c
Faulkes, David J.
deb5b229-ba15-407e-a9a7-f8af69dabf12
Diss, James K.
321de9b3-e7ec-488f-adff-779c8cd9c38f
Knight, Richard
76cd0c41-511b-475a-af63-938b74ef8270
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db

Carroll, Christopher J., Suleman, Naushaad, Davidson, Sean M., Faulkes, David J., Diss, James K., Knight, Richard, Stephanou, Anastasis, Latchman, David S. and Townsend, Paul A. (2011) Transgenic overexpression of HSP56 does not result in cardiac hypertrophy nor protect from ischaemia/reperfusion injury. International Journal of Biochemistry & Cell Biology, 43 (1), 74-79. (doi:10.1016/j.biocel.2010.09.020). (PMID:20932935)

Record type: Article

Abstract

Heat shock proteins are known to be induced during and following different forms of cardiac stress. It has previously been shown that their expression is beneficial for the heart following trauma such as ischaemia–reperfusion (I/R) injury. Heat shock protein 56 (HSP56) belongs to the family of FK506-binding immunophilin proteins and is found in steroid receptor complexes, notably the glucocorticoid receptor. We have previously shown that HSP56 and other HSPs are induced in cardiac myocytes treated with cardiotrophin-1, a cytokine with potent hypertrophic and protective properties on cardiac cells. The hypertrophic action of cardiotrophin-1 on cardiac cells is dependent on HSP56 induction and overexpression of HSP56 is sufficient for inducing hypertrophy in cardiac cells. To investigate this phenomenon in vivo, we have generated transgenic mice overexpressing HSP56 and assessed them for the development cardiac hypertrophy and resistance of their hearts to I/R-injury by Langendorff perfusion. Mice generated demonstrated stable, yet varying expression levels of HSP56. Initial characterisation identified a sex-specific phenotype where male overexpressing mice exhibited a moderate, but significant, reduced body weight compared to wild-type controls. In ex vivo stress analyses we found, unexpectedly, that significant overexpression of HSP56 does not induce myocardial hypertrophy and nor does it protect the intact heart from I/R-injury. These observations now suggest a more intricate HSP56-Sp. Cardiophenotype that requires further studies to determine if HSP56 is necessary in mediating hypertrophy induced by other myocardial stimuli.

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Accepted/In Press date: 4 October 2010
Published date: January 2011

Identifiers

Local EPrints ID: 169283
URI: https://eprints.soton.ac.uk/id/eprint/169283
ISSN: 1357-2725
PURE UUID: ca2fb92a-936b-4bed-b60b-29a8266b56ff

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Date deposited: 13 Dec 2010 14:36
Last modified: 18 Jul 2017 12:19

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Contributors

Author: Christopher J. Carroll
Author: Naushaad Suleman
Author: Sean M. Davidson
Author: David J. Faulkes
Author: James K. Diss
Author: Richard Knight
Author: Anastasis Stephanou
Author: David S. Latchman
Author: Paul A. Townsend

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