× Didn't find what you were looking for? Ask a question
Top Posters
Since Sunday
g
3
3
2
J
2
p
2
m
2
h
2
s
2
r
2
d
2
l
2
a
2
New Topic  
CarbonRobot CarbonRobot
wrote...
Posts: 393
Rep: 8 0
A year ago
Just in general what is wrong with older cells behaving young again? I was talking to an epigenetics expert (I assume) about how Yamanaka factors may make cells behave young again and cause some regenerations to occur. I suppose overactive cells with older DNA might prompt someone to worry that the chances of cancer are then higher. But in general are young acting older cells a good thing? Perhaps there are techniques to keep anything bad from happening?
Read 193 times
5 Replies

Related Topics

Replies
wrote...
Educator
A year ago
I've never heard of this phenomenon. Could you forward an article that explains it a bit more detail?
CarbonRobot Author
wrote...
A year ago
I've never heard of this phenomenon. Could you forward an article that explains it a bit more detail?

https://hms.harvard.edu/news/vision-revision

I don't understand what prompts regeneration in particular, but this technique seems to reverse the behaviors of cells to a more youthful ones.
wrote...
Educator
A year ago
Interesting read. Most important parts summarized below.

Lead study author Yuancheng Lu, research fellow in genetics at HMS and a former PhD student in Sinclair’s lab, developed a gene therapy that could safely reverse the age of cells in a living animal.

Lu’s work builds on the Nobel Prize-winning discovery of Shinya Yamanaka, who identified the four transcription factors, Oct4, Sox2, Klf4 and c-Myc, that could erase epigenetics markers on cells and return these cells to their primitive embryonic state from which they can develop into any other type of cell.

Subsequent studies, however, showed two important setbacks. First, when used in adult mice, the four Yamanaka factors could also induce tumor growth, rendering the approach unsafe. Second, the factors could reset the cellular state to the most primitive cell state, thus completely erasing a cell’s identity.

Lu and colleagues circumvented these hurdles by slightly modifying the approach. They dropped the gene c-Myc and delivered only the remaining three Yamanaka genes, Oct4, Sox2 and Klf4.  The modified approach successfully reversed cellular aging without fueling tumor growth or losing their identity.

The treatment resulted in a two-fold increase in the number of surviving retinal ganglion cells after the injury and a five-fold increase in nerve regrowth.

“At the beginning of this project, many of our colleagues said our approach would fail or would be too dangerous to ever be used,” said Lu. “Our results suggest this method is safe and could potentially revolutionize the treatment of the eye and many other organs affected by aging.”

Quote
Just in general what is wrong with older cells behaving young again?

I thought of an analogy of working on an old car. If you change the wheels of an old vehicle that has engine problems, putting brand new tires and rims won't make it run any better. Thus, if we end up repairing the cells of the eyes leading them to function like new again, perhaps all the blood vessels and neurons that lead to the eye are old and inefficient too. Hence, the new cells in the eye won't get the nutrients it needs to sustain its updated physiology.
CarbonRobot Author
wrote...
A year ago
Interesting read. Most important parts summarized below.
Lead study author Yuancheng Lu, research fellow in genetics at HMS and a former PhD student in Sinclair’s lab, developed a gene therapy that could safely reverse the age of cells in a living animal. Lu’s work builds on the Nobel Prize-winning discovery of Shinya Yamanaka, who identified the four transcription factors, Oct4, Sox2, Klf4 and c-Myc, that could erase epigenetics markers on cells and return these cells to their primitive embryonic state from which they can develop into any other type of cell. Subsequent studies, however, showed two important setbacks. First, when used in adult mice, the four Yamanaka factors could also induce tumor growth, rendering the approach unsafe. Second, the factors could reset the cellular state to the most primitive cell state, thus completely erasing a cell’s identity. Lu and colleagues circumvented these hurdles by slightly modifying the approach. They dropped the gene c-Myc and delivered only the remaining three Yamanaka genes, Oct4, Sox2 and Klf4. The modified approach successfully reversed cellular aging without fueling tumor growth or losing their identity.
The treatment resulted in a two-fold increase in the number of surviving retinal ganglion cells after the injury and a five-fold increase in nerve regrowth. “At the beginning of this project, many of our colleagues said our approach would fail or would be too dangerous to ever be used,” said Lu. “Our results suggest this method is safe and could potentially revolutionize the treatment of the eye and many other organs affected by aging.”
Quote
Just in general what is wrong with older cells behaving young again?
I thought of an analogy of working on an old car. If you change the wheels of an old vehicle that has engine problems, putting brand new tires and rims won't make it run any better. Thus, if we end up repairing the cells of the eyes leading them to function like new again, perhaps all the blood vessels and neurons that lead to the eye are old and inefficient too. Hence, the new cells in the eye won't get the nutrients it needs to sustain its updated physiology.

There is nothing to say that the cells from start to finish of a process like sight can't all be renewed? Retina, optic nerve, brain regions associated with sight? I don't think they're saying repair one part only if they can't even measure patient improvements because they still can't see well.

I think mitochondria malfunction is thought to be a major indicator of cellular age and decreased function. I am hopeful they can fix mitochondria issues as I believe it might be the first biological structure we've been able to represent in a 3D model.
wrote...
Educator
A year ago Edited: A year ago, bio_man
There is nothing to say that the cells from start to finish of a process like sight can't all be renewed? Retina, optic nerve, brain regions associated with sight? I don't think they're saying repair one part only if they can't even measure patient improvements because they still can't see well.

From the article it states:

The treatment resulted in a two-fold increase in the number of surviving retinal ganglion cells after the injury and a five-fold increase in nerve regrowth.

Which to me implies that the measure at which the retinal ganglion cells increase is indicative of eye health improvement. In fact, earlier in the article, it states:

To test whether the regenerative capacity of young animals could be imparted to adult mice, the researchers delivered the modified three-gene combination via an AAV into retinal ganglion cells of adult mice with optic nerve injury.

I'm not sure whether or not the repair went beyond repairing nerve injury; maybe more details are found in the actual article. If not, then is falls back to my original hypothesis that "perhaps all the blood vessels and neurons that lead to the eye [will still be] old and inefficient too."

Quote
I think mitochondria malfunction is thought to be a major indicator of cellular age and decreased function. I am hopeful they can fix mitochondria issues as I believe it might be the first biological structure we've been able to represent in a 3D model.

Certainly organelles such as mitochondria play a major role in the aging process. Mitochondrial DNA volume, integrity and functionality due to accumulation of mutations and oxidative damage is inversely proportional to advanced aging.
New Topic      
Explore
Post your homework questions and get free online help from our incredible volunteers
  1155 People Browsing
 139 Signed Up Today
Related Images
  
 176
  
 332
  
 165
Your Opinion
What's your favorite funny biology word?
Votes: 328