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001-es BibID:	BIBFORM060928
035-os BibID:	(WoS)000373072800283 (Scopus)84960114767
Első szerző:	Kovács Dóra (Biológus)
Cím:	Sebocytes differentially express and secrete adipokines / Dóra Kovács, Marianna Lovászi, Szilárd Póliska, Attila Oláh, Tamás Bíró, Imre Veres, Christos C. Zouboulis, Mona Ståhle, Ralph Rühl, Éva Remenyik, Dániel Törőcsik
Dátum:	2016
ISSN:	0906-6705
Megjegyzések:	In addition to producing sebum, sebocytes link lipid metabolism with inflammation at a cellular level and hence, greatly resemble adipocytes. However, so far no analysis was performed to identify and characterize the adipocyte-associated inflammatory proteins, the members of the adipokine family in sebocytes. Therefore, we determined the expression profile of adipokines (adiponectin, interleukin [IL] 6, resistin, leptin, serpin E1, visfatin, apelin, chemerin, retinol-binding protein 4 [RBP4] and monocyte chemoattractant protein 1 [MCP1]) in sebaceous glands of healthy and various disease-affected (acne, rosacea, melanoma and psoriasis) skin samples. Sebaceous glands in all examined samples expressed adiponectin, IL6, resistin, leptin, serpin E1 and visfatin, but not apelin, chemerin, RBP4 and MCP1. Confirming the presence of the detected adipokines in the human SZ95 sebaceous gland cell line we further characterized their expression and secretion patterns under different stimuli mimicking bacterial invasion (by using Toll-like receptor [TLR] 2 and 4 activators), or by 13-cis retinoic acid (13CRA; also known as isotretinoin), a key anti-acne agent. With the exception of resistin, the expression of all of the detected adipokines (adiponectin, IL6, leptin, serpin E1 and visfatin) could be further regulated at the level of gene expression, showing a close correlation with the secreted protein levels. Besides providing further evidence on similarities between adipocytes and sebocytes, our results strongly suggest that sebocytes are not simply targets of inflammation but may exhibit initiatory and modulatory roles in the inflammatory processes of the skin through the expression and secretion of adipokines.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Adipokine Inflammation Sebocyte
Megjelenés:	Experimental Dermatology. - 25 : 3 (2016), p. 194-199. -
További szerzők:	Lovászi Marianna (1986-) (biológus) Póliska Szilárd (1978-) (biológus) Oláh Attila (1984-) (élettanász) Bíró Tamás (1968-) (élettanász) Veres Imre (1963-) (bőrgyógyász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Ståhle, Mona Rühl, Ralph (1969-) (vegyész) Remenyik Éva (1956-) (bőrgyógyász) Töröcsik Dániel (1979-) (bőrgyógyász)
Pályázati támogatás:	NN117020 OTKA TÁMOP-4.2.2.A-11/1/KONV-2012-0031 TÁMOP TÁMOP-4.2.4 A/2-11-1-2012-0001 TÁMOP FP7-PEOPLE-2013-IEF Egyéb "Lendület" LP2011-003/2015 Egyéb
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001-es BibID:	BIBFORM116512
035-os BibID:	(Scopus)85180437359 (cikkazonosító)e14988 (WoS)001128766100001
Első szerző:	Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:	Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes and suppresses their endothelin release / Tóth Kinga Fanni, Ádám Dorottya, Arany József, Ramirez Yesid A., Bíró Tamás, Jennifer I. Drake, Alison O'Mahony, Szöllősi Attila Gábor, Póliska Szilárd, Ana Kilic, Michael Soeberdt, Christoph Abels, Oláh Attila
Dátum:	2024
ISSN:	0906-6705
Megjegyzések:	Fluoxetine is a safe antidepressant with remarkable anti-inflammatory actions; therefore, we aimed to investigate its effects on immortalized (HaCaT) as well as primary human epidermal keratinocytes in a polyinosinic-polycytidylic acid (p(I:C))-induced inflammatory model. We found that a non-cytotoxic concentration (MTT-assay, CyQUANT-assay) of fluoxetine significantly suppressed p(I:C)-induced expression and release of several pro-inflammatory cytokines (Q-PCR, cytokine array, ELISA), and it decreased the release of the itch mediator endothelins (ELISA). These effects were not mediated by the inhibition of the NF-?B or p38 MAPK pathways (western blot), or by the suppression of the p(I:C)-induced elevation of mitochondrial ROS production (MitoSOX Red labeling). Instead, unbiased activity profiling revealed that they were most likely mediated via the inhibition of the phosphoinositide 3-kinase (PI3K) pathway. Importantly, the PI3K-inhibitor GDC0941 fully mimicked the effects of fluoxetine (Q-PCR, ELISA). Although fluoxetine was able to occupy the binding site of GDC0941 (in silico molecular docking), and exerted direct inhibitory effect on PI3K (cell-free PI3K activity assay), it exhibited much lower potency and efficacy as compared to GDC0941. Finally, RNA-Seq analysis revealed that fluoxetine deeply influenced the transcriptional alterations induced by p(I:C)-treatment, and exerted an overall anti-inflammatory activity. Collectively, our findings demonstrate that fluoxetine exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via interfering with the PI3K pathway. Thus, clinical studies are encouraged to explore whether the currently reported beneficial effects translate in vivo following its topical administration in inflammatory and pruritic dermatoses.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk atopic dermatitis fluoxetine PI3K Toll-like receptor 3 inflammation keratinocyte itch endothelin
Megjelenés:	Experimental Dermatology. - 33 : 1 (2024), p. 1-15. -
További szerzők:	Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Póliska Szilárd (1978-) (biológus) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00015 GINOP GINOP-2.3.3-15-2016-00020 GINOP EFOP-3.6.3-VEKOP-16-2017-00009 EFOP NKFIH 125055 Egyéb NKFIH 134235 Egyéb NKFIH 134993 Egyéb János Bolyai Research Scholarship MTA ÚNKP-22-5-DE-427 Egyéb ÚNKP-23-5-DE-477 Egyéb TKP2021-NKTA-34 Egyéb Deutscher Akademischer Austauschdienst Egyéb Dr. August Wolff GmbH & Co. KG Arzneimittel Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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