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Transcriptional changes following restoration of SERCA2a levels in failing rat hearts
Author(s) -
Monte Federica,
Dalal Rishikesh,
Tabchy Adel,
Couget Jennifer,
Bloch Kenneth D.,
Peterson Randall,
Hajjar Roger J.
Publication year - 2004
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.04-1714fje
Subject(s) - heart failure , contractility , endoplasmic reticulum , intracellular , microarray , microbiology and biotechnology , gene , homeostasis , biology , medicine , gene expression , endocrinology , chemistry , biochemistry
Heart failure is characterized at the cellular level by impaired contractility and abnormal Ca 2+ homeostasis. We have previously shown that restoration of a key enzyme that controls intracellular Ca 2+ handling, the sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a), induces functional improvement in heart failure. We used high‐density oligonucleotide arrays to explore the effects of gene transfer of SERCA2a on genetic reprogramming in a model of heart failure. A total of 1,300 transcripts were identified to be unmodified by the effect of virus alone. Of those, 251 transcripts were found to be up‐ or down‐regulated upon failure. A total of 51 transcripts which were either up‐ (27) or down‐ (24) regulated in heart failure were normalized to the nonfailing levels by the restoration of SERCA2a by gene transfer. The microarray analysis identified new genes following SERCA2a restoration in heart failure, which will give us insights into their role in the normalization of multiple pathways within the failing cell.