To the naked eye, the blood, the only liquid tissue in the body, is a red flowing liquid. On closer examination with a microscope, this red liquid is observed to contain cells including the erythrocytes, leukocytes, and platelets. Like all cells, blood cells die; however, the body continues to replace them owing to the presence of certain undifferentiated cells known as stem cells and via a process known as hematopoiesis. Despite the seemingly abundant supply of blood stem cells, at old age, like most cells, the stem cells also become old, inactive, and eventually die. This inevitable death which plagues all cells including the stem cells begs the question, “When does aging begin?” For years, countless people have attempted to answer this simple yet nerve-racking question. While some believe that aging begins at some stage in life, others opine that for each cell, the aging process begins right from the moment of formation of that cell.
Genetic studies carried out by scientists at Fritz Lipmann Institute (FLI) in Jena, Germany may have successfully answered this question which seems to hold the key to many life’s mysteries. The study theories that the aging process is preprogrammed in the genetic makeup of the cell. Interestingly, the Igf2bp2 gene, the gene in which the aging program is encoded in stem cells, proved to be the same gene that controls growth and developmental processes in blood stem cells.
The Igf2bp2 gene; A controller of growth and an initiator of the aging process
The study performed using mice showed that the Igf2bp2 gene encodes the Igf2bp2 growth factor which controls stem cell function in growing stem cells by activating metabolism and growth. However, over time, this gene is silenced and loses its function. This loss of function was associated with the aging of the cells bearing the silenced genes.
Interestingly, mice cells that possessed mutated forms of the Igf2bp2 gene showed diminished levels of aging-associated loss of function despite the silencing of these genes.
They postulated that the activity phase of the Igf2bp2 gene at a youthful age may trigger some form of memory in the blood stem cell which drives the aging process later in life. Dr. Miaomiao Suo, the study’s first author, added that chemical changes in genetics or epigenetics may play a significant role in the entire process.
This study presents us with a dicey yet clinically applicable situation. Since we now know that aging is dependent on growth. We age because we grow. This is the harsh fact of life. However, by erasing the cellular memory of metabolic and growth activities we may be able to retard or even stop the aging process. This will greatly improve health and wellbeing.
This study proves that the aging process in blood stem cells (also known as hematopoietic stem cells) is not spontaneous. In contrast, it has already been programmed by their gene-driven growth in youth. However, although this study provides a clear explanation for one of the humanities’ most asked questions, it also brings forth another question, “By what mechanisms do epigenetic and genetic changes affect the Igf2bp2 gene for aging?”