Mitochondria are the major sites where energy is produced in the cell. Functions of organs such as the heart which has high energy demand are seriously affected by dysfunction of mitochondria. The functional changes in energy-dependent organs such as heart due to aging or any other cause are expected to be reflected in changes in expression of genes related to mitochondrial structure and function. Conversely, alteration of mitochondrial gene expression by any reason may also adversely affect function of organs such as heart that are energy-dependent. Molecular profiling of mitochondrial gene expression is therefore critical to understanding the mechanism of organ dysfunction. Mitochondrial structure and function are controlled by genes in the nuclear DNA and those in the mitochondrial DNA (mtDNA). The transcriptome from these two sources, together, contributing to the structure and function of mitochondria may be called mitoscriptome. This review elaborates on data gathered using a gene chip, RoMitochip, developed in our laboratory to study mitochondrial functional alteration in cardiomyocytes and left ventricular tissue following hypoxia or hemorrhagic injury. RoMitochip consists of probesets representing genes from nuclear DNA and mtDNA of both mice and rats. Our experiments using this chip in in vitro model of hypoxia and in vivo hemorrhagic injury model determined mitoscriptome signatures following hypoxia and hemorrhage, respectively. In addition, we also discuss past initiatives from other investigators that led to the development of microarray tools to profile mitoscriptome.
