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Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
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Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
J Biomed Sci. 2022 Mar 7;29(1):17. doi: 10.1186/s12929-022-00800-7.
Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
Young Hyun Jung # 1, Chang Woo Chae # 1, Gee Euhn Choi # 1, Him Cha Shin 2, Jae Ryong Lim 1, Han Seung Chang 1, Joonmo Park 1, Ji Hyeon Cho 1, Mo Ran Park 1, Hyun Jik Lee 3 4, Ho Jae Han 5
Background: Androgenetic alopecia (AGA) is a genetic disorder caused by dihydrotestosterone (DHT), accompanied by the senescence of androgen-sensitive dermal papilla cells (DPCs) located in the base of hair follicles. DHT causes DPC senescence in AGA through mitochondrial dysfunction. However, the mechanism of this pathogenesis remains unknown. In this study, we investigated the protective role of cyanidins on DHT-induced mitochondrial dysfunction and DPC senescence and the regulatory mechanism involved.
Methods: DPCs were used to investigate the effect of DHT on mitochondrial dysfunction with MitoSOX and Rhod-2 staining. Senescence-associated β-galactosidase activity assay was performed to examine the involvement of membrane AR-mediated signaling in DHT-induced DPC senescence. AGA mice model was used to study the cyanidins on DHT-induced hair growth deceleration.
Results: Cyanidin 3-O-arabinoside (C3A) effectively decreased DHT-induced mtROS accumulation in DPCs, and C3A reversed the DHT-induced DPC senescence. Excessive mitochondrial calcium accumulation was blocked by C3A. C3A inhibited p38-mediated voltage-dependent anion channel 1 (VDAC1) expression that contributes to mitochondria-associated ER membrane (MAM) formation and transfer of calcium via VDAC1-IP3R1 interactions. DHT-induced MAM formation resulted in increase of DPC senescence. In AGA mice models, C3A restored DHT-induced hair growth deceleration, which activated hair follicle stem cell proliferation.
Conclusions: C3A is a promising natural compound for AGA treatments against DHT-induced DPC senescence through reduction of MAM formation and mitochondrial dysfunction.
Keywords: Androgen receptor; Cyanidin 3-O-arabinoside; DHT; Mitochondrial calcium; Senescence.
Full Study:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8900350/
Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
Young Hyun Jung # 1, Chang Woo Chae # 1, Gee Euhn Choi # 1, Him Cha Shin 2, Jae Ryong Lim 1, Han Seung Chang 1, Joonmo Park 1, Ji Hyeon Cho 1, Mo Ran Park 1, Hyun Jik Lee 3 4, Ho Jae Han 5
Background: Androgenetic alopecia (AGA) is a genetic disorder caused by dihydrotestosterone (DHT), accompanied by the senescence of androgen-sensitive dermal papilla cells (DPCs) located in the base of hair follicles. DHT causes DPC senescence in AGA through mitochondrial dysfunction. However, the mechanism of this pathogenesis remains unknown. In this study, we investigated the protective role of cyanidins on DHT-induced mitochondrial dysfunction and DPC senescence and the regulatory mechanism involved.
Methods: DPCs were used to investigate the effect of DHT on mitochondrial dysfunction with MitoSOX and Rhod-2 staining. Senescence-associated β-galactosidase activity assay was performed to examine the involvement of membrane AR-mediated signaling in DHT-induced DPC senescence. AGA mice model was used to study the cyanidins on DHT-induced hair growth deceleration.
Results: Cyanidin 3-O-arabinoside (C3A) effectively decreased DHT-induced mtROS accumulation in DPCs, and C3A reversed the DHT-induced DPC senescence. Excessive mitochondrial calcium accumulation was blocked by C3A. C3A inhibited p38-mediated voltage-dependent anion channel 1 (VDAC1) expression that contributes to mitochondria-associated ER membrane (MAM) formation and transfer of calcium via VDAC1-IP3R1 interactions. DHT-induced MAM formation resulted in increase of DPC senescence. In AGA mice models, C3A restored DHT-induced hair growth deceleration, which activated hair follicle stem cell proliferation.
Conclusions: C3A is a promising natural compound for AGA treatments against DHT-induced DPC senescence through reduction of MAM formation and mitochondrial dysfunction.
Keywords: Androgen receptor; Cyanidin 3-O-arabinoside; DHT; Mitochondrial calcium; Senescence.
Full Study:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8900350/
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bobbers2011 likes this post
Re: Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
Can C3A be readily purchased anywhere?
bobbers2011- Posts : 28
Join date : 2011-12-23
Location : UK
Re: Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts
bobbers2011 wrote:Can C3A be readily purchased anywhere?
Most of the supplements mentioned in this thread contain it
https://immortalhair.forumotion.com/t13364-serum-paroxonase-1-level-may-be-an-indicator-and-predictor-of-the-severity-of-androgenetic-alopecia
_________________
My regimen
http://www.immortalhair.org/mpb-regimen
Now available for consultation (hair and/or health)
http://www.immortalhair.org/health-consultation
bobbers2011 likes this post
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