Endogenous retroviruses (ERVs) play an important role in the expression regulation of many animal and human genes and are involved in the processes of transcriptional and posttranscriptional editing. ERVs retain a certain genetic similarity to the exogenous generic virus. ERV research helps to determine the age and rate of evolution of exogenous viruses that are contagious to animals and humans. It is hypothesized that retroviruses arose before the appearance of vertebrates. This asynchrony suggests a significant contribution of retroviruses to the evolutionary development of organisms. ERVs have no species boundaries due to horizontal transfer; however, the movement of retrotransposons in the genome of animals can lead to cytogenetic defects and have a negative effect on the fitness of organisms. One striking example of horizontal transfer is the LINE 1 retrotransposon, which was found in 559 species, including animals, plants, and fungi. This confirms the assumption about the time of the emergence of retroviruses. Retrotransposons, which participate in the processes of transposition and recombination, cause changes in DNA nucleotide sequences. This leads to mutational processes in genes, in particular, those responsible for the development of neurons in the brain and nervous system, i.e., retrotransposons may be responsible for domestication syndrome. The infection of germ cells with retroviruses gradually led to their establishment of reproductive functions in mammals. These functions include the fusion of trophoblasts in the placenta. ERV genes are incorporated into the genome via viral infections or retrotransposition. The review systematizes and summarizes the knowledge of the evolution and transfer of ERVs in the body and their functions in the genome and describes the main and most common ERVs, as well as their molecular structure and properties.
The published data on the regulation of telomerase activity are systemized. The structure and functions of telomeres and telomerase are described. The main pathways of epigenetic regulation of telomerase activity—modification of the TERT (telomerase reserve transcriptase) gene histone and its methylation— are described. Particular attention is paid to the regulation of telomerase activity at the transcriptional level (transcriptional activators and inhibitors of TERT, as well as two-way transcription regulators) and posttranscriptional regulation (alternative splicing of TERT mRNA, phosphorylation, and ubiquitination of TERT).
We studied the protective effect of bioregulators isolated from the liver and blood serum of mammals under conditions of manifest fibrosis. Fibrosis was induced by CCl 4 administration for 30 days and then, the liver was cultured in a roller organotypic culture for 30 days in the presence of bioregulators. Hepatoprotective effect of bioregulators was evaluated on histological sections of the liver at different terms of culturing. Experiments with roller organotypic culture of the liver isolated from animals with in vivo CCl 4 -induced fibrosis demonstrated the protective effect of bioregulator of the liver origin, while bioregulator isolated from the blood was ineffective.
Поиск новых путей терапии заболеваний печени остается актуальной проблемой биологии и медицины на сегодняшний день. В настоящей работе были исследованы два пептидно-белковых комплекса, принадлежащих к группе мембранотропных гомеостатических тканеспецифических биорегуляторов, выделенных из печени и сыворотки крови млекопитающих. Представлена краткая характеристика физико-химических свойств данных комплексов: состав пептидов и белков, входящих в данные комплексы, исследование их вторичной структуры, образование ими наноразмерных частиц в растворе. На модели CCl4 индуцированного фиброза печени мыши было исследовано протекторное действие изучаемых комплексов. Показано, что биорегулятор, выделенный из сыворотки крови, не проявлял гепатопротекторную активность, а биорегулятор, выделенный из печени, на фоне токсического повреждения печени мыши снижал темпы развития индуцированного фиброза.