Xuesong Zhang1, Dongmei Zhou1,2, Tengfei Ma1, Qingquan Liu1,2. 1. Department of Dermatology, Beijing Shunyi Hospital of Traditional Chinese Medicine, Shunyi District, Beijing, China. 2. Department of Dermatology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Dongcheng District, Beijing, China.
Abstract
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 (AGA) patients and the apoptosis of HFSCs may be involved in the pathogenesis of AGA. The expression of Vascular endothelial growth factor (VEGF) turns to be weakened or disappeared in hair follicles of AGA patients. OBJECTIVE: To investigate whether VEGF is involved in the apoptosis of HFSCs induced by 5α-DHT in the patients of AGA. 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.
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 (AGA) patients and the apoptosis of HFSCs may be involved in the pathogenesis of AGA. The expression of Vascular endothelial growth factor (VEGF) turns to be weakened or disappeared in hair follicles of AGA patients. OBJECTIVE: To investigate whether VEGF is involved in the apoptosis of HFSCs induced by 5α-DHT in the patients of AGA. 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.