Vascular Endothelial Growth Factor Protects CD200-Rich and CD34-Positive Hair Follicle Stem Cells Against Androgen-Induced Apoptosis Through the Phosp

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Vascular Endothelial Growth Factor Protects CD200-Rich and CD34-Positive Hair Follicle Stem Cells Against Androgen-Induced Apoptosis Through the Phosphoinositide 3-Kinase/Akt Pathway in Patients With Androgenic Alopecia.​


Background: 5α-DHT can decrease the cell viability of the hair follicle stem cells (HFSCs) with CD34-positive and CD200-rich in bald scalp area of androgenic alopecia (Androgenetic Alopecia) patients and the apoptosis of HFSCs may be involved in the pathogenesis of Androgenetic Alopecia. The expression of Vascular endothelial growth factor (VEGF) turns to be weakened or disappeared in hair follicles of Androgenetic Alopecia patients.

Objective: To investigate whether VEGF is involved in the apoptosis of HFSCs induced by 5α-DHT in the patients of Androgenetic Alopecia.

Methods: By 5α-DHT, apoptosis of CD200-rich and CD34-positive HFSCs was induced and apoptotic rates up to 24 hours were assessed using flow cytometry. The expression grades of Bcl-2, Akt, caspase-3 and Bax were observed through Western blot analysis.

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.

 

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Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.​


Abstract​

Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia.
 
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KNemo

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LouisSarkozy

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Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.​


Abstract​

Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia.
does vegf causes skin aging i know minoxidil increases vegf but do you think vegf on itself would lead to wrinkles?
 
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