Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near?
- Thread starter yassin
- Start date
2020
Experienced Member
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- 50
and I said: no **** bald people have less progenitor cells... that's like saying that people with missing fingers have less progenitor cells. Obvious is obvious. Tiny follicles -> less cells.
the problem is not the AMOUNT OF PROGENITOR CELLS, it's the fact that those remaining stem cells(which last forever) no longer PRODUCE progenitor cells(temporary).
squeegee
Banned
- Reaction score
- 132
I LOL
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Endothelial progenitor cells (EPCs) are decreased in number in a chronic inflammatory environment. Period.
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[h=1]Inhibition of cyclooxygenase (COX)-2 affects endothelial progenitor cell proliferation.[/h]Colleselli D, Bijuklic K, Mosheimer BA, Kähler CM.
[h=3]Source[/h]Pneumology Service-Division of General Internal Medicine, Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria.
[h=3]Abstract[/h]Growing evidence indicates that inducible cyclooxygenase-2 (COX-2) is involved in the pathogenesis of inflammatory disorders and various types of cancer. Endothelial progenitor cells recruited from the bone marrow have been shown to be involved in the formation of new vessels in malignancies and discussed for being a key point in tumour progression and metastasis. However, until now, nothing is known about an interaction between COX and endothelial progenitor cells (EPC). Expression of COX-1 and COX-2 was detected by semiquantitative RT-PCR and Western blot. Proliferation kinetics, cell cycle distribution and rate of apoptosis were analysed by MTT test and FACS analysis. Further analyses revealed an implication of Akt phosphorylation and caspase-3 activation. Both COX-1 and COX-2 expression can be found in bone-marrow-derived endothelial progenitor cells in vitro. COX-2 inhibition leads to a significant reduction in proliferation of endothelial progenitor cells by an increase in apoptosis and cell cycle arrest. COX-2 inhibition leads further to an increased cleavage of caspase-3 protein and inversely to inhibition of Akt activation. Highly proliferating endothelial progenitor cells can be targeted by selective COX-2 inhibition in vitro. These results indicate that upcoming therapy strategies in cancer patients targeting COX-2 may be effective in inhibiting tumour vasculogenesis as well as angiogenic processes.
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Prostaglandins have profound effects on Progenitor cell
[h=1]Prostaglandin E positively modulates endothelial progenitor cell homeostasis: an advanced treatment modality for autologous cell therapy.[/h]Herrler T, Leicht SF, Huber S, Hermann PC, Schwarz TM, Kopp R, Heeschen C.
[h=3]Source[/h]Department of Surgery, Experimental Medicine, Ludwig Maximilian University, Munich, Germany.
[h=3]Abstract[/h][h=4]AIMS:[/h]The mobilization of endothelial progenitor cells (EPC) and their functioning in postnatal neovascularization are tightly regulated. To identify new modulators of EPC homeostasis, we screened biologically active prostaglandin E compounds for their effects on EPC production, trafficking and function.
[h=4]METHODS AND RESULTS:[/h]We found that EPC are a rich source for prostaglandin E(2) (PGE(2)), stimulating their number and function in an auto- and paracrine manner. In vivo blockade of PGE(2) production by selective cyclooxygenase-2 inhibition virtually abrogated ischemia-induced EPC mobilization demonstrating its crucial role in EPC homeostasis following tissue ischemia. Conversely, ex vivo treatment of isolated EPC with the clinically approved PGE(1) analogue alprostadil enhanced EPC number and function. These effects were mediated by increased expression of the chemokine receptor CXCR4 and were dependent on nitric oxide synthase activity. Most importantly, ex vivo PGE(1) pretreatment of isolated EPC significantly enhanced their neovascularization capacity in a murine model of hind limb ischemia as assessed by laser Doppler analysis, exercise stress test and immunohistochemistry.
[h=4]CONCLUSIONS:[/h]The conserved role for PGE in the regulation of EPC homeostasis suggests that ex vivo modulation of the prostaglandin pathway in isolated progenitor cells may represent a novel and safe strategy to facilitate cell-based therapies.
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Endothelial progenitor cells (EPCs) are decreased in number in a chronic inflammatory environment. Period.
- - - Updated - - -
[h=1]Inhibition of cyclooxygenase (COX)-2 affects endothelial progenitor cell proliferation.[/h]Colleselli D, Bijuklic K, Mosheimer BA, Kähler CM.
[h=3]Source[/h]Pneumology Service-Division of General Internal Medicine, Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria.
[h=3]Abstract[/h]Growing evidence indicates that inducible cyclooxygenase-2 (COX-2) is involved in the pathogenesis of inflammatory disorders and various types of cancer. Endothelial progenitor cells recruited from the bone marrow have been shown to be involved in the formation of new vessels in malignancies and discussed for being a key point in tumour progression and metastasis. However, until now, nothing is known about an interaction between COX and endothelial progenitor cells (EPC). Expression of COX-1 and COX-2 was detected by semiquantitative RT-PCR and Western blot. Proliferation kinetics, cell cycle distribution and rate of apoptosis were analysed by MTT test and FACS analysis. Further analyses revealed an implication of Akt phosphorylation and caspase-3 activation. Both COX-1 and COX-2 expression can be found in bone-marrow-derived endothelial progenitor cells in vitro. COX-2 inhibition leads to a significant reduction in proliferation of endothelial progenitor cells by an increase in apoptosis and cell cycle arrest. COX-2 inhibition leads further to an increased cleavage of caspase-3 protein and inversely to inhibition of Akt activation. Highly proliferating endothelial progenitor cells can be targeted by selective COX-2 inhibition in vitro. These results indicate that upcoming therapy strategies in cancer patients targeting COX-2 may be effective in inhibiting tumour vasculogenesis as well as angiogenic processes.
- - - Updated - - -
Prostaglandins have profound effects on Progenitor cell
[h=1]Prostaglandin E positively modulates endothelial progenitor cell homeostasis: an advanced treatment modality for autologous cell therapy.[/h]Herrler T, Leicht SF, Huber S, Hermann PC, Schwarz TM, Kopp R, Heeschen C.
[h=3]Source[/h]Department of Surgery, Experimental Medicine, Ludwig Maximilian University, Munich, Germany.
[h=3]Abstract[/h][h=4]AIMS:[/h]The mobilization of endothelial progenitor cells (EPC) and their functioning in postnatal neovascularization are tightly regulated. To identify new modulators of EPC homeostasis, we screened biologically active prostaglandin E compounds for their effects on EPC production, trafficking and function.
[h=4]METHODS AND RESULTS:[/h]We found that EPC are a rich source for prostaglandin E(2) (PGE(2)), stimulating their number and function in an auto- and paracrine manner. In vivo blockade of PGE(2) production by selective cyclooxygenase-2 inhibition virtually abrogated ischemia-induced EPC mobilization demonstrating its crucial role in EPC homeostasis following tissue ischemia. Conversely, ex vivo treatment of isolated EPC with the clinically approved PGE(1) analogue alprostadil enhanced EPC number and function. These effects were mediated by increased expression of the chemokine receptor CXCR4 and were dependent on nitric oxide synthase activity. Most importantly, ex vivo PGE(1) pretreatment of isolated EPC significantly enhanced their neovascularization capacity in a murine model of hind limb ischemia as assessed by laser Doppler analysis, exercise stress test and immunohistochemistry.
[h=4]CONCLUSIONS:[/h]The conserved role for PGE in the regulation of EPC homeostasis suggests that ex vivo modulation of the prostaglandin pathway in isolated progenitor cells may represent a novel and safe strategy to facilitate cell-based therapies.
LawOfThelema
Experienced Member
- Reaction score
- 18
the hair at the back and sides don't fall off partly because there are few androgen receptors in that area. it has been found experimentally that balding scalps have a higher distribution of ARs in the balding areas, particularly at the vertex and the crown, compared to non-balding controls, and compared to nonbalding areas of the scalp.
odalbak
Established Member
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- 11
Sources?
baldnesssadness
Established Member
- Reaction score
- 4
thanks for answering my question now im only waiting for sources, ive found cetirizin ratiopharm 10 mg which i used some time ago for allergies. how can i use to minimize pgd2 in my body? should i just take it orally or mix it together with minoxidil? i wanna use it oraly because pgd2 also caused sebaceous glands to increase which i feel is getting more in my body, i cant give sources by this but its in the forum somewhere i read it. Squeegee you and boldy are one of the best forum posters u give facts which is more important that theories.
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but why does the hair in the back stay for as long as you live? what makes it stay? i believe if we found out why they are there which stem cell or whatever makes it stay we could maybe grow back hair in the areas that are bald.
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but why does the hair in the back stay for as long as you live? what makes it stay? i believe if we found out why they are there which stem cell or whatever makes it stay we could maybe grow back hair in the areas that are bald.
2020
Experienced Member
- Reaction score
- 50
lol what? I'm right.
Are you suggesting that somehow blocking COX-2 would allow stem cells to start producing progenitor cells again?
squeegee
Banned
- Reaction score
- 132
Inflammation induces release of progenitor cells. Circulating EPC contribute to normal hair growth. Lowering both Cox isoform will lower inflammation and contribute to hair growth. Also adding any nitric oxide booster like Minoxidil and Miconazole Nitrate will also contribute to the releases and migration of EPC. This is the recipe to reverse hairloss. Numerous degenerative conditions are associated with production of inflammatory mediators, which directly suppress EPC production or activity. I considered hairloss as degenerative skin condition.. the increased demand for de novo EPC production in inflammatory conditions would theoretically lead to exhaustion of EPC precursors cells by virtue of telomere shortening......
LawOfThelema
Experienced Member
- Reaction score
- 18
hi
i have been following this tread for sometime and have done a little google research myself. I wanted to share this to get your thoughts. Applogies if it has been discussed before.
Structural and functional characterization of HQL-79, an orally selective inhibitor of human hematopoietic prostaglandin D synthase.
AbstractWe determined the crystal structure of human hematopoietic prostaglandin (PG) D synthase (H-PGDS) as the quaternary complex with glutathione (GSH), Mg2+, and an inhibitor, HQL-79, having anti-inflammatory activities in vivo, at a 1.45-A resolution. In the quaternary complex, HQL-79 was found to reside within the catalytic cleft between Trp104 and GSH. HQL-79 was stabilized by interaction of a phenyl ring of its diphenyl group with Trp104 and by its piperidine group with GSH and Arg14 through water molecules, which form a network with hydrogen bonding and salt bridges linked to Mg2+. HQL-79 inhibited human H-PGDS competitively against the substrate PGH2 and non-competitively against GSH with Ki of 5 and 3 microm, respectively. Surface plasmon resonance analysis revealed that HQL-79 bound to H-PGDS with an affinity that was 12-fold higher in the presence of GSH and Mg2+ (Kd, 0.8 microm) than in their absence. Mutational studies revealed that Arg14 was important for the Mg2+-mediated increase in the binding affinity of H-PGDS for HQL-79, and that Trp104, Lys112, and Lys198 were important for maintaining the HQL-binding pocket. HQL-79 selectively inhibited PGD2 production by H-PGDS-expressing human megakaryocytes and rat mastocytoma cells with an IC50 value of about 100 microm but only marginally affected the production of other prostanoids, suggesting the tight functional engagement between H-PGDS and cyclooxygenase. Orally administered HQL-79 (30 mg/kg body weight) inhibited antigen-induced production of PGD2, without affecting the production of PGE2 and PGF2alpha, and ameliorated airway inflammation in wild-type and human H-PGDS-overexpressing mice. Knowledge about this structure of quaternary complex is useful for understanding the inhibitory mechanism of HQL-79 and should accelerate the structure-based development of novel anti-inflammatory drugs that inhibit PGD2 production specifically.
http://www.jbc.org/content/281/22/15277.full.pdf
HQL-79 is selective in inhibiting the pathway that converts Arachadonic acid into PGD2, however it has little effect on the other prostoglandins according to this study.
I recall somewhere in the Cotseralis patent the mention of this but not much discussion on it elsewhere, well not that i could find.
i have been following this tread for sometime and have done a little google research myself. I wanted to share this to get your thoughts. Applogies if it has been discussed before.
Structural and functional characterization of HQL-79, an orally selective inhibitor of human hematopoietic prostaglandin D synthase.
AbstractWe determined the crystal structure of human hematopoietic prostaglandin (PG) D synthase (H-PGDS) as the quaternary complex with glutathione (GSH), Mg2+, and an inhibitor, HQL-79, having anti-inflammatory activities in vivo, at a 1.45-A resolution. In the quaternary complex, HQL-79 was found to reside within the catalytic cleft between Trp104 and GSH. HQL-79 was stabilized by interaction of a phenyl ring of its diphenyl group with Trp104 and by its piperidine group with GSH and Arg14 through water molecules, which form a network with hydrogen bonding and salt bridges linked to Mg2+. HQL-79 inhibited human H-PGDS competitively against the substrate PGH2 and non-competitively against GSH with Ki of 5 and 3 microm, respectively. Surface plasmon resonance analysis revealed that HQL-79 bound to H-PGDS with an affinity that was 12-fold higher in the presence of GSH and Mg2+ (Kd, 0.8 microm) than in their absence. Mutational studies revealed that Arg14 was important for the Mg2+-mediated increase in the binding affinity of H-PGDS for HQL-79, and that Trp104, Lys112, and Lys198 were important for maintaining the HQL-binding pocket. HQL-79 selectively inhibited PGD2 production by H-PGDS-expressing human megakaryocytes and rat mastocytoma cells with an IC50 value of about 100 microm but only marginally affected the production of other prostanoids, suggesting the tight functional engagement between H-PGDS and cyclooxygenase. Orally administered HQL-79 (30 mg/kg body weight) inhibited antigen-induced production of PGD2, without affecting the production of PGE2 and PGF2alpha, and ameliorated airway inflammation in wild-type and human H-PGDS-overexpressing mice. Knowledge about this structure of quaternary complex is useful for understanding the inhibitory mechanism of HQL-79 and should accelerate the structure-based development of novel anti-inflammatory drugs that inhibit PGD2 production specifically.
http://www.jbc.org/content/281/22/15277.full.pdf
HQL-79 is selective in inhibiting the pathway that converts Arachadonic acid into PGD2, however it has little effect on the other prostoglandins according to this study.
I recall somewhere in the Cotseralis patent the mention of this but not much discussion on it elsewhere, well not that i could find.
Koga
Established Member
- Reaction score
- 37
Anyone tried onion (juice)? How about mixing onion juice with some alcohol and applying it every night? Should block PGD2 and mimic PGE2.. And the stuff I read about castor oil: shouldn't be 'the' solution, but still a great growth stimulant, no? And quercetin, ginger, aspirin..?
odalbak
Established Member
- Reaction score
- 11
Man… There's been so many suggestions in such a long thread, more than 700 posts now. And how many have actually tried something on their hair? This looks like the thread for guys more interested in hair science than their hair itself.
Koga
Established Member
- Reaction score
- 37
That's exactly my point. Too bad, there's a lot of motivated people here but most are waiting on experiences that ain't coming.. I might give the onion juice a shot. What could be the harm in pouring some alcohol and onion on your head for a few months, right?
we are currently waiting for OC000459 production, and we are testing Valporic Acid( to stimulate CD progenitor cells)+ as well the WNT signaling pathway.
things just takes time and in the meantime its good to discuss new opportunities that might work more efficient.
see hairlosshelp for reference.
things just takes time and in the meantime its good to discuss new opportunities that might work more efficient.
see hairlosshelp for reference.
baldnesssadness
Established Member
- Reaction score
- 4
ive been using cetirizine for the last 6 days and before that i had so much itching on my head, everywhere was itching specially my hairline it was like it was burning . after i started with cetirizine my itching is minimal and allmost to nothing when i showered today i diddnt shower these 6 days because i wanted to see if i lost extra hair while showering, nothing much really it was some but less then before im sure it takes time to make pgd2 levels shrink , i lost minimal to normal hair average daily right now i will start combing my hair more i have receeded a bit on the hairline thou but im gonna stay optimisitic i use 30 mg daily? i wont go more than that ? boldy do you think i should go lower? no im only feeling a bit tired thats my side effect. Damn 2020 i have to say your in every pgd2 thread out there and you are allways arguing with someone.
Started today... not experiencing any side effects. I experienced heavy hay fever and decided to take 2 pills (10mg). The hay fever disappeared after two hours and for the rest no strange effects. Not sure if I am going to take 2 every day or only one.
If you get tired as a side effect it could be an idea to take it in the evening before going to bed.
Some good news. A few years ago (2004) on the dutch hairloss forum (haarweb) there was a big discussion on antihistamine for hairloss. Many experienced hair growth after a very short period. They mainly used cetrizine! Although many were not sure and very skeptical if it was because of cetrizine since there was no scientific proof. It is a very big topic: http://www.haarweb.nl/forum/showthread. ... ihistamine (use google translate to read it) Many experienced results after a very short period. I believe all users only used 1 pill (10mg)
Did you see any results?
I mean Boldy.... sorry. Could you answer me? Thanks.