Aging process - Balancing the process of new self-renewal and aging

US scientists have asked the same basic question about the aging process: why do the original cells lose the ability to divide and create new cells?

Research by three research groups found that the protein called p16 ^INK4a limits the ability of aging cells to produce new cells in the bone marrow, brain and pancreas. The activity of p16 ^INK4a increases as the original cells lose the ability to replicate new cells.

(Artwork: SinhhocVietNam) The p16 ^INK4a protein is the main product from the encoding of INK4, also known as p16 ^INK4a cancer suppressor protein. This protein plays a role in regulating the cell cycle in the form of binding and inactivating different types of CDK rings. The expression of p16 ^INK4a will increase with age and this expression process is related to the aging process of the cell and is recognized as dominant to the aging process. As you get older, the concentration of p16 ^INK4a will be higher.

Morrison's team at the University of Michigan studied neuronal cells located in the anterior brain region of mice. Sharpless and colleagues from North Carolina University studied the original cells in Langerhans island involving beta cells that secrete insulin. The third group of Scadden from Harvard Medical University experimented on the cells that make up the bone marrow. These three studies were published in Nature.

All three research groups created mice lacking p16 ^INK4a protein and then conducted surveys when they got older. The original cells in mice did not show the usual decline due to aging. The lack of p16INK4a protein causes stem cells to function normally as if they were not aging. The natural aging process has a balance between the aging process of cells and the ability to self-renew cells (dividing and creating new cells).

The authors predict that the expression of p16 ^INK4a protein may have been programmed to suit growth. The amount of p16INK4a protein increases with aging to counteract the increased effect of cancer in aging cells. Alternatively, an increase in the expression of p16 ^INK4a protein may reflect the deterioration of aging cells in response to the increasing risk of aging cells.

Researchers also suggest that type 2 diabetes (a non-insulin-dependent form) may partly be explained by pancreatic dysfunction during the creation of new cells with aging. Research results from cells with different origins such as bone marrow, pancreatic endocrine glands and brain showed that p16 ^INK4a dominated the aging process by limiting the self-renewal of the cells. planed cells can multiply. The role of p16 ^INK4a to control the balance between self-renewal and aging of the remaining tissues should continue to be studied.

Thai Khac Minh