After an acute myocardial infarction, millions of heart cells, called cardiomyocytes, die and are replaced by a scar. The heart tissue never recovers completely in mammals, such as humans; but in other animals, the repair can be total. This is the case of zebrafish, an animal model that shares most of its genes with humans.

A team of scientists from the Institute of Anatomy of the University of Bern (Switzerland) has been trying to understand the cellular mechanisms of the regeneration of the heart of the zebrafish for more than ten years. Together with the National Center for Cardiovascular Research (CNIC), La Paz Hospital in Madrid, the Bioinformatics Unit of the University of Bern and the European Laboratory of Molecular Biology Heidelberg (EMBL) in Germany have tested their hypotheses.

In a study published in the journal Cell Reports and led by the CNIC, researchers show that not all cardiomyocytes in the heart of the zebrafish contribute in the same way to regenerate lost muscle. Actually, a specific set of cells has greater regenerative capacity.

Greater cell repair

Thanks to the use of transgenic tools, Marcos Sande-Melón, a CNIC scientist and lead author of the study, and his colleagues, were able to identify a small subset of cardiomyocytes in the heart of the zebrafish marked by an expression of sox10 gene, which had expanded more than the rest of myocardial cells in response to injury.

These cells differed from the rest of the myocardium also in their gene expression profile, suggesting that they represented a particular group of cells. In addition, by experimentally erasing these small cells the regeneration of the heart was impaired.

We were able to identify a specific cell population that is more efficient than all other heart muscle cells during regeneration, and we show that their contribution to repair is essential,” says Nadia Mercader, co-author of research and scientist at the Swiss university.

The question that researchers now ask is whether this finding can stimulate the repair process in the human heart. Therefore, the next step will be to unravel the role of the sox10 gene in that special cell group.

We want to find out if the absence of this population of sox10 cells in mammals could explain why our heart does not regenerate well,” concludes Mercader.

 

Source: Agencia ID