Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression.

Abstract:

:Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved in the initiation of autoimmune, metabolic, and cardiovascular diseases. The role of HSP60 in pathogenesis of these diseases remains unclear, partly because of the lack of mouse models expressing HSP60. In this study we generated HSP60 conditional transgenic mice suitable for investigating in vivo outcomes by expressing HSP60 at the targeted organ in disease models. Ubiquitous HSP60 induction in the embryonic stage caused neonatal death in mice at postnatal day 1. A high incidence of atrial septal defects was observed in HSP60-expressing mice, with increased apoptosis and myocyte degeneration that possibly contributed to massive hemorrhage and sponge-like cardiac muscles. Our results showed that neonatal heart failure through HSP60 induction likely involves developmental defects and excessive apoptosis. The conditional HSP60 mouse model is useful for studying crucial biological questions concerning HSP60.

journal_name

Biomed Res Int

authors

Chen TH,Liu SW,Chen MR,Cho KH,Chen TY,Chu PH,Kao YY,Hsu CH,Lin KM

doi

10.1155/2015/539805

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

539805

eissn

2314-6133

issn

2314-6141

journal_volume

2015

pub_type

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