The death switch?
Blocking the mechanism of "suicide" of cells will overcome heart attack and strokeRIA News
Scientists have learned to block the mechanism of genetic damage control that triggers the cellular self-destruction program, which can contribute to the creation of drugs for heart attack and stroke, according to an article published in the journal Genes & Development (Jing Chen and Michael B. Kastan, 5'-3'-UTR interactions regulate p53 mRNA translation and provide a target for modulating p53 induction after DNA damage – VM).
The p53 protein plays a key role in protecting animal cells from genetic damage. In case of serious breakdowns in the genomic DNA molecule, p53 launches a program of apoptosis – cellular "suicide". In this way, in particular, the body is protected from the occurrence of cancerous tumors in it.
But apoptosis also has an undesirable side associated with mass cell death. Collective self-destruction of cells occurs in various ischemic conditions. Therefore, it is desirable to block apoptosis in heart and brain cells, which will help to treat the consequences of heart attack and stroke in humans more effectively.
Synthesis of the p53 protein in cells occurs when another protein, RPL26, binds to its matrix RNA (genetic "instruction"). In this case, the ends of a single-stranded RNA molecule are joined together, creating a short double-stranded section.
Molecular biologists from St. Jude Children's Research Hospital (Memphis, USA) have learned how to manage this process.
The scientists added short single-stranded DNA molecules to the cell culture, similar in structure to the free ends of the matrix RNA of the protein p53. Penetrating into the cells, DNA molecules bound to the molecules of this RNA. As a result, suppression of p53 protein synthesis was observed.
According to the researchers, the results of their work can lead to the creation of drugs that protect human organs from the negative effects of apoptosis. "Theoretically, it is possible to reduce the level of p53 in those tissues where it is necessary," explained the head of research Michael Kastan (Michael Kastan).
In the near future, scientists plan to start experiments to "turn off" the synthesis of p53 in mice. "The road to creating a medicine will be long. But on this path, we will be able to better understand the mechanism of interaction between RPL26 and the p53 matrix RNA. Perhaps we will find other small molecules capable of blocking this mechanism," concluded Castan.
Portal "Eternal youth" http://vechnayamolodost.ru15.09.2010