Vascular Endothelial Growth Factor Protects Cd200-rich And Cd34-positive Hair Follicle Stem Cells

[Otis Mack]

We know the numbers of CD200 and CD34 cells are low in Androgenetic Alopecia. Now we have a plausible reason of why that might be:


https://www.ncbi.nlm.nih.gov/pubmed/31478937


RESULTS:
Vascular endothelial growth factor could cut 5α-DHT induced apoptosis down substantially in a concentration-dependent manner. The 5α-DHT induced decline in the rise of Bcl-2/Bax proportion and the increase in caspase-3 degrees were mostly reversed by using VEGF and the VEGF's anti-apoptotic actions were impeded through preventing the activation of phosphoinositide 3-kinase (PI3K)/Akt.

CONCLUSION:
Vascular endothelial growth factor can protect CD200-rich and CD34-positive HFSCs from androgen induced apoptosis by means of the PI3K/Akt pathway.

 

[whatevr]

It's impossible to obtain VEGF anywhere except as one of those growth serums (Cellcurin etc.) and it's questionable if the dose is any good. Not much we can do about this one without knowing which pathway the DHT->VEGF inhibition happens and how to inhibit it.

 

[Otis Mack]

Just find molecules to stimulate VEGF production providing the cells are still capable of making it.

One of the best known ones is minoxidil:

https://www.ncbi.nlm.nih.gov/pubmed/9580790

 

[whatevr]

Just find molecules to stimulate VEGF production providing the cells are still capable of making it.

One of the best known ones is minoxidil:

https://www.ncbi.nlm.nih.gov/pubmed/9580790

Anything else? I've looked far and wide and only minoxidil and estrogenic compounds give the classic "puffy hair" effect of VEGF which can be seen and felt very quickly. Most of the herbal stuff which purports to increase VEGF (I think I tried gotu kola and some others) did nothing.

 

[Xander94]

these studies are confusing and contradicting and we will never get anything out of them. VEGF is inhibited by almost every antioxidant yet we know antioxidants help with hairloss when we test them on subjects.

We should use what we have and wait for the future ....

 

[Otis Mack]

these studies are confusing and contradicting and we will never get anything out of them. VEGF is inhibited by almost every antioxidant yet we know antioxidants help with hairloss when we test them on subjects.

We should use what we have and wait for the future ....

I dont think the study is confusing and certainly points out that VEGF is central to preventing Androgenetic Alopecia by mitigating dht's role in apoptosis in CD200 and CD34 cells and probably dermal papilla too altho the study didnt look at that.


Um...antioxidants. Yes can be useful but this triggers a long standing hypothesis of why inflammation IS important at least initially to trigger
anagen.

Inflammation drives autophagy which you will never have anagen without autophagy. Autophagy drives differentiation of stem cells to dermal papilla.

Antioxidants suppress autophagy because autophagy in itself is thought of as a ROS scavenging system. Alot of the autophagy works by blocking Caspase 1 formation.

Moral of the story: you CANNOT continually have either zero inflammation(which antioxidants lean towards) or chronic inflammation(as in Androgenetic Alopecia) as signalling gets screwed up.


You also cannot have continual autophagy either and treatments that "didnt work" too well may benefit from just some time off.

I will find some studies which show my above statement.


Also, anything(drug or any type of wounding) that grows hair first triggers autophagy....check it out.

 

[Otis Mack]

I dont think the study is confusing and certainly points out that VEGF is central to preventing Androgenetic Alopecia by mitigating dht's role in apoptosis in CD200 and CD34 cells and probably dermal papilla too altho the study didnt look at that.




You also cannot have continual autophagy either and treatments that "didnt work" too well may benefit from just some time off.

I will find some studies which show my above statement.

Could this be the reason nothing ever became of lactic acid? Were people allowing enough time in between applications?


https://www.ncbi.nlm.nih.gov/pubmed/26171114


L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial Dysfunction via Mitohormesis.
Zelenka J1, Dvořák A2, Alán L2.
Author information
1
Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, 142 20 Prague, Czech Republic ; Department of Biochemistry and Microbiology, Institute of Chemical Technology Prague, Technická 5, 166 28 Prague, Czech Republic.
2
Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, 142 20 Prague, Czech Republic.
Abstract
A moderate elevation of reactive oxygen species (ROS) production and a mild inhibition of mitochondrial respiratory chain have been associated with a health promotion and a lifespan extension in several animal models of aging.

Here, we tested whether this phenomenon called mitohormesis could be mediated by L-lactate.

The treatment with 5 mM L-lactate significantly increased H2O2 production and slightly inhibited the respiration in cultured skin fibroblasts and in isolated mitochondria. The L-lactate exposure was associated with oxidation of intracellular glutathione, phosphorylation of 5'AMP-activated protein kinase (AMPK), and induction of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) transcription.

A replicative aging of fibroblasts (L0) with a constant (LC), or intermittent 5 mM L-lactate (LI) in media showed that the high-passage LI fibroblasts have higher respiration, lower H2O2 release, and lower secretion of L-lactate compared to L0 and LC.

This protection against mitochondrial dysfunction in LI cells was associated with lower activity of mechanistic target of rapamycin complex 1 (mTORC1), less signs of cellular senescence, and increased autophagy compared to L0 and LC.

In conclusion, we demonstrated that intermittent but not constant exposure to L-lactate triggers mitohormesis, prevents aging-associated mitochondrial dysfunction, and improves other markers of aging.

 

[Xander94]

I dont think the study is confusing and certainly points out that VEGF is central to preventing Androgenetic Alopecia by mitigating dht's role in apoptosis in CD200 and CD34 cells and probably dermal papilla too altho the study didnt look at that.


Um...antioxidants. Yes can be useful but this triggers a long standing hypothesis of why inflammation IS important at least initially to trigger
anagen.

Inflammation drives autophagy which you will never have anagen without autophagy. Autophagy drives differentiation of stem cells to dermal papilla.

Antioxidants suppress autophagy because autophagy in itself is thought of as a ROS scavenging system. Alot of the autophagy works by blocking Caspase 1 formation.

Moral of the story: you CANNOT continually have either zero inflammation(which antioxidants lean towards) or chronic inflammation(as in Androgenetic Alopecia) as signalling gets screwed up.


You also cannot have continual autophagy either and treatments that "didnt work" too well may benefit from just some time off.

I will find some studies which show my above statement.


Also, anything(drug or any type of wounding) that grows hair first triggers autophagy....check it out.

Then we should supplement in a rythmic manner ?

What about mitochondrial dysfunction theory in scalp ?

 

[Otis Mack]

Then we should supplement in a rythmic manner ?

What about mitochondrial dysfunction theory in scalp ?

I would say dont over supplement antioxidants because they compete with autophagy. Autophagy ideally perfectly regulates ROS which are needed for cell proliferation.

Durk Pearson and Sandy Shaw were pioneers in supplements which were free radical scavengers. They took mega-doses of things which at
that time(20-30 years ago) looked scientifically very prudent to do. I saw pictures of them awhile back and they looked quite a bit older than they should've. The Morelife.org guy is a heavy supplement guy too and aint got no spring chicken look to him or his girlfriend either.

Mito dysfunction in Androgenetic Alopecia? Is it causal or just a consequence of? I say consequence of. There are studies of adolescents who get Androgenetic Alopecia too and they are pretty young. Is their mitochondria shot before they reach puberty? I doubt that...

 

[Xander94]

I would say dont over supplement antioxidants because they compete with autophagy. Autophagy ideally perfectly regulates ROS which are needed for cell proliferation.

Durk Pearson and Sandy Shaw were pioneers in supplements which were free radical scavengers. They took mega-doses of things which at
that time(20-30 years ago) looked scientifically very prudent to do. I saw pictures of them awhile back and they looked quite a bit older than they should've. The Morelife.org guy is a heavy supplement guy too and aint got no spring chicken look to him or his girlfriend either.

Mito dysfunction in Androgenetic Alopecia? Is it causal or just a consequence of? I say consequence of. There are studies of adolescents who get Androgenetic Alopecia too and they are pretty young. Is their mitochondria shot before they reach puberty? I doubt that...

Legit but maybe the mitochondria in the follicle are dysfunctioning and supplementing with pqq could protect them from prematurely becoming mutated.

By the way what supplements would you recommend ? I take a vitE tocotrienol supp daily should I stop that?

 

[Xander94]

PQQ suppresses literally everything thats high in balding scalps

http://atm.amegroups.com/article/view/29416/html

suppressing the Jak2/STAT3, TGF-β1/Smad3, JNK/p38 MAPK, and NF-κB signaling pathways.