Using comprehensive genetic analysis, a research group led by Professor Mitsuyoshi Nakao of Kumamoto University has clarified that the enzyme "NSD2" that blocks cell aging has a role in preventing cell aging.
Many cells that make up the body, when they divide repeatedly and increase, eventually lose their function and stop growing.This is called "cell aging" and is an important factor related to health and longevity.In recent years, attention has been focused on the function of senescent cells by secreting various proteins and acting on surrounding cells to promote chronic inflammation and the growth of cancer cells.Cellular senescence is being seen as the cause of aging throughout the body, and if cell aging can be controlled, it may be possible to regulate the progress of aging throughout the body.
The research group has been conducting research on the mechanism of cell aging, and has screened a wide range of factors involved in aging of human fibroblasts (cell types present in all tissues and organs) to date.This time, we have identified "NSD2 methyltransferase".
In the research, when a method of suppressing the action of the NSD2 gene (RNA interference method) was applied to fibroblasts, cell aging was induced and its typical characteristics appeared, so NSD2 has a role to prevent cell aging. Turned out.In addition, the decrease in NSD2 inactivated the function of genes involved in cell proliferation and stopped proliferation.Furthermore, it was found that cells normally proliferate by the action of proteins (growth factors) that promote proliferation in serum, which requires NSD2.
The protective factor for cellular senescence identified by the research group is the fourth in this research result. With the discovery that NSD4 protects against cellular aging, the basic mechanism of aging was clarified, and it is expected to be useful for elucidating the mechanism of aging and developing a control method that regulates the activity of enzymes.
Paper information:[Aging Cell] The NSD2 / WHSC1 / MMSET methyltransferase prevents cellular senescence-associated epigenomic remodeling