Heart failure and apoptosis: Electrophoretic methods support data from micro- and macro-arrays. A critical review of genomics and proteomics

Abstract

The multiple causes and multiple consequences of mammalian heart failure make it an attractive proposition for analysis using gene array technology, especially where the failure is idiopathic in nature. However, gene arrays also hold potential artefacts, particularly when gene expression levels are low, and where changes in expression levels are modest. Also, at present, the number of genes available on arrays is not large enough to prevent potential sampling deficiencies. Thus, it may not be wise to place too much reliance on quantitative interpretations of gene array data. Also, recently doubts were raised about the qualitative reliability of array genes. Electrophoretic methods are slow, cumbersome and complex but they can provide confirmation that the trends and numbers arising from the new gene arrays are reliable. In this overview, we compare gene array data with data from protein activity assays such as zymograms, Western blots, two-dimensional electrophoresis, and immunohistochemistry. Similar or complementary data from the same heart tissues analyzed by either microarrays or macroarrays can be reassuring to those interested in reliable molecular analyses of normal and failing hearts. Similar principles will apply to other tissues and cells.

Proteomics Strategies in Cardiovascular Research

“…[1][2][3][46][47][48] On the other hand, this work is meant to be a strategy paper, such that we describe a path toward:…”

“…Cardiovascular research has been one of the first successful applications of proteomic research. The pioneering work of Dunn et al [1][2][3][4] provides one of the examples of a global approach in studying molecular mechanisms in cardiovascular biology and medicine.…”

The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease

“…Mouse hearts retain a limited regenerative capacity but it was thought that not even low levels of mitosis occurred in human cardiomyocytes. Jiang et al (2001) critically reviewed the evidence for apoptosis in the human heart and concluded that apoptosis does occur, but at a very low rate. The field had to wait more than a decade for evidence that cell death was compensated for by cardiac proliferation (Mollova et al 2013;Polizzotti et al 2015).…”

Fosinopril and Carvedilol Reverse Hypertrophy and Change the Levels of Protein Kinase Cɛ and Components of its Signaling Complex

“…HFassociated cardiac proteins are mainly classified into the following functional systems: (1) mitochondria and energy production, (2) cytoskeletal proteins, (3) glycolytic enzymes related proteins [29]. To our knowledge, our research is the first to reveal altered proteins in cardiac PKC( complexes during the three stages of POH: POH with cardiac hypertrophy only, POH with HF and POH reversed with drugs, and especially the latter.…”