Cell proliferation limit and senescence (ES and fibroblasts)

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In summary, the difference in proliferation limits between ES cells and fibroblasts is an important factor to consider when engineering organs.
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Homework Statement


Hello,
I am trying to understand the importance of proliferation limits and cell senescence. In particular, one of my homework questions is asking to compare the proliferation limit of Embryonic Stem cells (ES) and fibroblasts (which would be trans-differentiated) and describe how this difference plays a role when thinking about engineering organs, for example a heart transplant.

Homework Equations


Hayflick limit for senescence is ~50 cell divisions.

The Attempt at a Solution


Here is what I am thinking, however I am not sure if this is correct or not.
Non-differentiated the ES cells can divide almost indefinitely, however when the stem cell differentiates into a specific function, it goes through approximately 50 cell divisions before senescence. On the other hand, fibroblasts have already gone through some cell divisions at the point when they are trans-differentiated. Therefore, their life before senescence is less than 50 cell divisions.

Can someone verify this? How do ES cells and fibroblasts compare with regards to the Hayflick limit?
Thank you.
 
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Yes, this is correct. Embryonic stem cells can divide almost indefinitely in their undifferentiated state, while fibroblasts have already gone through some cell divisions before they are trans-differentiated and therefore have a shorter life before senescence. The Hayflick limit for both ES cells and fibroblasts is approximately 50 cell divisions. This difference plays an important role when it comes to engineering organs such as a heart transplant. For example, since ES cells have a much longer life before senescence, they can be used to produce more cells necessary for a successful transplant. On the other hand, fibroblasts have a shorter life before senescence, so they may not be able to produce as many cells as ES cells.
 

FAQ: Cell proliferation limit and senescence (ES and fibroblasts)

1. What is cell proliferation limit?

Cell proliferation limit refers to the maximum number of times a cell can divide before it stops dividing and enters a state of senescence or cell death. This limit is determined by the number of times a cell's DNA can replicate without errors, as well as other factors such as telomere shortening and oxidative stress.

2. What is senescence?

Senescence is a state in which a cell stops dividing and undergoes changes that lead to its eventual death. This process can be triggered by various factors, including DNA damage, telomere shortening, and cellular stress. Senescent cells can no longer contribute to tissue growth and repair, and can even have negative effects on surrounding cells.

3. How does cell proliferation limit differ between embryonic stem cells and fibroblasts?

Embryonic stem cells have a much higher proliferation limit compared to fibroblasts. This is because embryonic stem cells have the ability to continuously self-renew and maintain their undifferentiated state, while fibroblasts have a limited number of divisions before reaching senescence. Additionally, embryonic stem cells have the ability to repair and maintain their telomeres, which helps to prevent the accumulation of DNA damage.

4. Can cell proliferation limit be extended?

Research has shown that the proliferation limit of cells can be extended by manipulating certain genes and cellular pathways. For example, the enzyme telomerase can be activated to prevent telomere shortening and prolong the lifespan of cells. However, there are potential risks associated with extending the proliferation limit of cells, such as increased risk of cancer.

5. How does cell proliferation limit play a role in aging?

As cells reach their proliferation limit and enter senescence, they can no longer contribute to tissue repair and maintenance. This can lead to age-related decline and increased susceptibility to diseases and disorders. Additionally, the accumulation of senescent cells can have negative effects on surrounding cells and tissues, contributing to the aging process. Therefore, understanding and potentially manipulating cell proliferation limit may play a crucial role in addressing age-related issues.

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