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Dátum csökkenő
1.
001-es BibID:
BIBFORM048815
Első szerző:
Langan, Ewan A.
Cím:
Tumour necrosis factor alpha, interferon gamma and substance P are novel modulators of extrapituitary prolactin expression in human skin / Ewan A. Langan, Silvia Vidali, Natascha Pigat, Wolfgang Funk, Erika Lisztes, Tamás Bíró, Vincent Goffin, Christopher E. M. Griffiths, Ralf Paus
Dátum:
2013
ISSN:
1932-6203
Megjegyzések:
Human scalp skin and hair follicles (HFs) are extra-pituitary sources of prolactin (PRL). However, the intracutaneous regulation of PRL remains poorly understood. Therefore we investigated whether well-recognized regulators of pituitary PRL expression, which also impact on human skin physiology and pathology, regulate expression of PRL and its receptor (PRLR) in situ. This was studied in serum-free organ cultures of microdissected human scalp HFs and skin, i.e. excluding pituitary, neural and vascular inputs. Prolactin expression was confirmed at the gene and protein level in human truncal skin, where its expression significantly increased (p?=?0.049) during organ culture. There was, however, no evidence of PRL secretion into the culture medium as measured by ELISA. PRL immunoreactivity (IR) in female human epidermis was decreased by substance P (p?=?0.009), while neither the classical pituitary PRL inhibitor, dopamine, nor corticotropin-releasing hormone significantly modulated PRL IR in HFs or skin respectively. Interferon (IFN) ? increased PRL IR in the epithelium of human HFs (p?=?0.044) while tumour necrosis factor (TNF) ? decreased both PRL and PRLR IR. This study identifies substance P, TNF? and IFN? as novel modulators of PRL and PRLR expression in human skin, and suggests that intracutaneous PRL expression is not under dopaminergic control. Given the importance of PRL in human hair growth regulation and its possible role in the pathogenesis of several common skin diseases, targeting intracutaneous PRL production via these newly identified regulatory pathways may point towards novel therapeutic options for inflammatory dermatoses.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:
PLoS One. - 8 : 4 (2013), p. e60819. -
További szerzők:
Vidali, Silvia
Pigat, Natascha
Funk, Wolfgang
Lisztes Erika (1986-) (élettanász)
Bíró Tamás (1968-) (élettanász)
Goffin, Vincent
Griffiths, Christopher E. M.
Paus, Ralf
Internet cím:
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
2.
001-es BibID:
BIBFORM085361
035-os BibID:
(WoS)000537309400001 (Scopus)85085880838
Első szerző:
Oláh Attila (élettanász)
Cím:
Mitochondrial energy metabolism is negatively regulated by cannabinoid receptor 1 in intact human epidermis / Oláh Attila, Alam Majid, Chéret Jérémy, Kis Nikoletta Gréta, Hegyi Zoltán, Szöllősi Attila Gábor, Vidali Silvia, Bíró Tamás, Paus Ralf
Dátum:
2020
ISSN:
0906-6705
Megjegyzések:
Epidermal energy metabolism is relevant to skin physiology, aging, and photodamage. While selected hormones stimulate epidermal keratinocyte mitochondrial activity, its negative regulation remains unknown. In several cell types, cannabinoid receptor 1 (CB1) is expressed both in the cell membrane (cmCB1), and in the mitochondrial outer membrane (mtCB1), where its stimulation directly suppresses mitochondrial functions. In the current pilot study, we investigated if CB1 is a negative regulator of human epidermal energy metabolism under physiological conditions. Using organ-cultured full-thickness human skin specimens of healthy individuals, we showed that antagonizing the homeostatic CB1 signaling by the administration of the CB1 inverse agonist AM251 increased activity of respiratory chain complex I and II/IV activity in a CB1-dependent manner, since the CB1-selective agonist arachidonyl-2'-chloroethylamide could prevent the effect. Moreover, the phenomenon was also reproduced by siRNA-mediated down-regulation of CB1. As revealed by the unaltered expression of several relevant markers (TFAM, VDAC1, MTCO1, and NDUFS4), modulation of CB1 signaling had no effect on the epidermal mitochondrial mass. Next, by using immunoelectron microscopy, we found that human epidermal keratinocytes express both cmCB1 and mtCB1. Finally, by using equipotent extracellularly-restricted (hemopressin) as well as cell-permeable (AM251) inverse agonists, we found that mitochondrial activity is most likely exclusively regulated by mtCB1. Thus, our data identify mtCB1 as a negative regulator of keratinocyte mitochondrial activity in intact human epidermis, and highlight the question, whether topical therapeutic interventions capable of selectively activating mtCB1 can reduce excessive mitochondrial ROS production resulting from dysregulated mitochondrial activity during skin aging or photodamage.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
endocannabinoid
epidermal keratinocyte
mitochondrial activity
mitochondrially expressed CB1 (mtCB1)
cannabinoid receptor 1 (CB1)
Megjelenés:
Experimental Dermatology. - 29 : 7 (2020), p. 616-622. -
További szerzők:
Alam, Majid
Chéret, Jérémy
Kis Gréta (1979-) (környezetkutató)
Hegyi Zoltán (1983-) (molekuláris biológus)
Szöllősi Attila Gábor (1982-) (élettanász)
Vidali, Silvia
Bíró Tamás (1968-) (élettanász)
Paus, Ralf
Pályázati támogatás:
121360
OTKA
125055
OTKA
Hungarian National Brain Research Program [KTIA_NAP_13-1-2013-001]
Egyéb
Bolyai János Kutatási Ösztöndíj
MTA
ITM - Új Nemzeti Kiválóság Program ÚNKP-19-4-DE-287
Egyéb
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
3.
001-es BibID:
BIBFORM048833
035-os BibID:
PMID:23949722
Első szerző:
Vidali, Silvia
Cím:
Hypothalamic-Pituitary-Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles / Silvia Vidali, Jana Knuever, Johannes Lerchner, Melanie Giesen, Tamás Bíró, Matthias Klinger, Barbara Kofler, Wolfgang Funk, Burkhard Poeggeler, Ralf Paus
Dátum:
2014
ISSN:
0022-202X
Megjegyzések:
Thyroid hormones regulate mitochondrial function. As other hypothalamic-pituitary-thyroid (HPT) axis hormones, i.e., thyrotropin-releasing hormone (TRH) and thyrotropin (TSH), are expressed in human hair follicles (HFs) and regulate mitochondrial function in human epidermis, we investigated in organ-cultured human scalp HFs whether TRH (30?nM), TSH (10?mU?ml-1), thyroxine (T4) (100?nM), and triiodothyronine (T3) (100?pM) alter intrafollicular mitochondrial energy metabolism. All HPT-axis members increased gene and protein expression of mitochondrial-encoded subunit 1 of cytochrome c oxidase (MTCO1), a subunit of respiratory chain complex IV, mitochondrial transcription factor A (TFAM), and Porin. All hormones also stimulated intrafollicular complex I/IV activity and mitochondrial biogenesis. The TSH effects on MTCO1, TFAM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-mediated action. Notably, as measured by calorimetry, T3 and TSH increased follicular heat production, whereas T3/T4 and TRH stimulated ATP production in cultured HF keratinocytes. HPT-axis hormones did not increase reactive oxygen species (ROS) production. Rather, T3 and T4 reduced ROS formation, and all tested HPT-axis hormones increased the transcription of ROS scavengers (catalase, superoxide dismutase 2) in HF keratinocytes. Thus, mitochondrial biology, energy metabolism, and redox state of human HFs are subject to profound (neuro-)endocrine regulation by HPT-axis hormones. The neuroendocrine control of mitochondrial biology in a complex human mini-organ revealed here may be therapeutically exploitable.
Tárgyszavak:
Orvostudományok
Klinikai orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
Calcium (Ca2+) signalling
Ion channel
Membrane transport
Molecular mechanisms of disease
Skin
TRP channels
Megjelenés:
Journal of Investigative Dermatology. - 134 (2014), p. 33-42. -
További szerzők:
Knüver, Jana
Lerchner, Johannes
Giesen, Melanie
Bíró Tamás (1968-) (élettanász)
Klinger, Matthias
Kofler, Barbara
Funk, Wolfgang
Poeggeler, Burkhard
Paus, Ralf
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
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