Inhibition of human hair follicle growth by endo- and exocannabinoids.

Standard

Inhibition of human hair follicle growth by endo- and exocannabinoids. / Telek, Andrea; Bíró, Tamás; Bodó, Eniko; Tóth, Balázs I; Borbíró, István; Kunos, George; Paus, Ralf.

in: FASEB J, Jahrgang 21, Nr. 13, 13, 2007, S. 3534-3541.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Telek, A, Bíró, T, Bodó, E, Tóth, BI, Borbíró, I, Kunos, G & Paus, R 2007, 'Inhibition of human hair follicle growth by endo- and exocannabinoids.', FASEB J, Jg. 21, Nr. 13, 13, S. 3534-3541. <http://www.ncbi.nlm.nih.gov/pubmed/17567570?dopt=Citation>

APA

Telek, A., Bíró, T., Bodó, E., Tóth, B. I., Borbíró, I., Kunos, G., & Paus, R. (2007). Inhibition of human hair follicle growth by endo- and exocannabinoids. FASEB J, 21(13), 3534-3541. [13]. http://www.ncbi.nlm.nih.gov/pubmed/17567570?dopt=Citation

Vancouver

Telek A, Bíró T, Bodó E, Tóth BI, Borbíró I, Kunos G et al. Inhibition of human hair follicle growth by endo- and exocannabinoids. FASEB J. 2007;21(13):3534-3541. 13.

Bibtex

@article{fd1a51368e304098ba435c25838ec485,
title = "Inhibition of human hair follicle growth by endo- and exocannabinoids.",
abstract = "Recent studies strongly suggest that the cannabinoid system is a key player in cell growth control. Since the organ-culture of human hair follicles (HF) offers an excellent, clinically relevant model for complex tissue interaction systems, we have asked whether the cannabinoid system plays a role in hair growth control. Here, we show that human scalp HF, intriguingly, are both targets and sources of endocannabinoids. Namely, the endocannabinoid N-arachidonoylethanolamide (anandamide, AEA) as well as the exocannabinnoid delta (9) -tetrahydrocannabinol dose-dependently inhibited hair shaft elongation and the proliferation of hair matrix keratinocytes, and induced intraepithelial apoptosis and premature HF regression (catagen). These effects were inhibited by a selective antagonist of cannabinoid receptor-1 (CB1). In contrast to CB2, CB1 was expressed in a hair cycle-dependent manner in the human HF epithelium. Since we successfully identified the presence of endocannabinoids in human HF, our data strongly suggest that human HF exploit a CB1-mediated endocannabinoid signaling system for negatively regulating their own growth. Clinically, CB1 agonists may therefore help to manage unwanted hair growth, while CB1 antagonists might counteract hair loss. Finally, human HF organ culture offers an instructive, physiologically relevant new research tool for dissecting {"}nonclassical{"} effects of endocannabinoids and their receptor-mediated signaling in general.",
author = "Andrea Telek and Tam{\'a}s B{\'i}r{\'o} and Eniko Bod{\'o} and T{\'o}th, {Bal{\'a}zs I} and Istv{\'a}n Borb{\'i}r{\'o} and George Kunos and Ralf Paus",
year = "2007",
language = "Deutsch",
volume = "21",
pages = "3534--3541",
journal = "FASEB J",
issn = "0892-6638",
publisher = "FASEB",
number = "13",

}

RIS

TY - JOUR

T1 - Inhibition of human hair follicle growth by endo- and exocannabinoids.

AU - Telek, Andrea

AU - Bíró, Tamás

AU - Bodó, Eniko

AU - Tóth, Balázs I

AU - Borbíró, István

AU - Kunos, George

AU - Paus, Ralf

PY - 2007

Y1 - 2007

N2 - Recent studies strongly suggest that the cannabinoid system is a key player in cell growth control. Since the organ-culture of human hair follicles (HF) offers an excellent, clinically relevant model for complex tissue interaction systems, we have asked whether the cannabinoid system plays a role in hair growth control. Here, we show that human scalp HF, intriguingly, are both targets and sources of endocannabinoids. Namely, the endocannabinoid N-arachidonoylethanolamide (anandamide, AEA) as well as the exocannabinnoid delta (9) -tetrahydrocannabinol dose-dependently inhibited hair shaft elongation and the proliferation of hair matrix keratinocytes, and induced intraepithelial apoptosis and premature HF regression (catagen). These effects were inhibited by a selective antagonist of cannabinoid receptor-1 (CB1). In contrast to CB2, CB1 was expressed in a hair cycle-dependent manner in the human HF epithelium. Since we successfully identified the presence of endocannabinoids in human HF, our data strongly suggest that human HF exploit a CB1-mediated endocannabinoid signaling system for negatively regulating their own growth. Clinically, CB1 agonists may therefore help to manage unwanted hair growth, while CB1 antagonists might counteract hair loss. Finally, human HF organ culture offers an instructive, physiologically relevant new research tool for dissecting "nonclassical" effects of endocannabinoids and their receptor-mediated signaling in general.

AB - Recent studies strongly suggest that the cannabinoid system is a key player in cell growth control. Since the organ-culture of human hair follicles (HF) offers an excellent, clinically relevant model for complex tissue interaction systems, we have asked whether the cannabinoid system plays a role in hair growth control. Here, we show that human scalp HF, intriguingly, are both targets and sources of endocannabinoids. Namely, the endocannabinoid N-arachidonoylethanolamide (anandamide, AEA) as well as the exocannabinnoid delta (9) -tetrahydrocannabinol dose-dependently inhibited hair shaft elongation and the proliferation of hair matrix keratinocytes, and induced intraepithelial apoptosis and premature HF regression (catagen). These effects were inhibited by a selective antagonist of cannabinoid receptor-1 (CB1). In contrast to CB2, CB1 was expressed in a hair cycle-dependent manner in the human HF epithelium. Since we successfully identified the presence of endocannabinoids in human HF, our data strongly suggest that human HF exploit a CB1-mediated endocannabinoid signaling system for negatively regulating their own growth. Clinically, CB1 agonists may therefore help to manage unwanted hair growth, while CB1 antagonists might counteract hair loss. Finally, human HF organ culture offers an instructive, physiologically relevant new research tool for dissecting "nonclassical" effects of endocannabinoids and their receptor-mediated signaling in general.

M3 - SCORING: Zeitschriftenaufsatz

VL - 21

SP - 3534

EP - 3541

JO - FASEB J

JF - FASEB J

SN - 0892-6638

IS - 13

M1 - 13

ER -