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001-es BibID:BIBFORM098747
035-os BibID:(cikkazonosító)21510 (WOS)000714953500017 (Scopus)85118421272
Első szerző:Dull Katalin (molekuláris biológus, genetikus)
Cím:miR-146a modulates TLR1/2 and 4 induced inflammation and links it with proliferation and lipid production via the indirect regulation of GNG7 in human SZ95 sebocytes / Dull Katalin, Fazekas Fruzsina, Deák Dávid, Kovács Dóra, Póliska Szilárd, Szegedi Andrea, Zouboulis Christos C., Törőcsik Dániel
Dátum:2021
ISSN:2045-2322
Megjegyzések:Activation of Toll-like receptors (TLR) 1/2 and 4 are central in inducing inflammation in sebocytes by regulating the expression of protein coding mRNAs, however the microRNA (miRNA) profile in response to TLR activation and thus the possible role of miRNAs in modulating sebocyte functions has not been elucidated. In this work we identified miR-146a to have the highest induction in the TLR1/2 and 4 activated SZ95 sebocytes and found that its increased levels led to the down-regulation of IL-8 secretion, decreased the chemoattractant potential and stimulated the proliferation of sebocytes. Assessing the gene expression profile of SZ95 sebocytes treated with a miR-146a inhibitor, the induction of GNG7 was one of the highest, while when cells were treated with a miR-146a mimic, the expression of GNG7 was down-regulated. These findings correlated with our in situ hybridization results, that compared with control, miR-146a showed an increased, while GNG7 a decreased expression in sebaceous glands of acne samples. Further studies revealed, that when inhibiting the levels of GNG7 in SZ95 sebocytes, cells increased their lipid content and decreased their proliferation. Our findings suggest, that miR-146a could be a potential player in acne pathogenesis by regulating inflammation, inducing proliferation and, through the indirect down-regulation of GNG7, promoting the lipid production of sebocytes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Scientific Reports. - 11 : 1 (2021), p. 1-13. -
További szerzők:Fazekas Fruzsina (1993-) (biológus) Deák Dávid Kovács Dóra (1988-) (Biológus) Póliska Szilárd (1978-) (biológus) Szegedi Andrea (1964-) (bőrgyógyász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Töröcsik Dániel (1979-) (bőrgyógyász)
Pályázati támogatás:FK-132296
OTKA
K-128250
OTKA
GINOP-2.3.2-15-2016- 00005
GINOP
EFOP-3.6.1-16-2016-00022
EFOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM089467
035-os BibID:(cikkazonosító)9048 (scopus)85096802734 (wos)000597487400001
Első szerző:Kovács Dóra (Biológus)
Cím:Adipokines in the Skin and in Dermatological Diseases / Kovács Dóra, Fazekas Fruzsina, Oláh Attila, Törőcsik Dániel
Dátum:2020
ISSN:1661-6596 1422-0067
Megjegyzések:Adipokines are the primary mediators of adipose tissue-induced and regulated systemic inflammatory diseases; however, recent findings revealed that serum levels of various adipokines correlate also with the onset and the severity of dermatological diseases. Importantly, further data confirmed that the skin serves not only as a target for adipokine signaling, but may serve as a source too. In this review, we aim to provide a complex overview on how adipokines may integrate into the (patho) physiological conditions of the skin by introducing the cell types, such as keratinocytes, fibroblasts, and sebocytes, which are known to produce adipokines as well as the signals that target them. Moreover, we discuss data from in vivo and in vitro murine and human studies as well as genetic data on how adipokines may contribute to various aspects of the homeostasis of the skin, e.g., melanogenesis, hair growth, or wound healing, just as to the pathogenesis of dermatological diseases such as psoriasis, atopic dermatitis, acne, rosacea, and melanoma.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
adipokines
keratinocytes
fibroblasts
sebocytes
melanocytes; hair growth
psoriasis
atopic dermatitis
acne
melanoma
Megjelenés:International Journal Of Molecular Sciences. - 23 : 21 (2020), p. 9048. -
További szerzők:Fazekas Fruzsina (1993-) (biológus) Oláh Attila (1984-) (élettanász) Töröcsik Dániel (1979-) (bőrgyógyász)
Pályázati támogatás:Egyéb
OTKA
GINOP-2.3.2-15-2016-00005
GINOP
Új Nemzeti Kiválóság Program
Egyéb
Egyéb
MTA
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM094083
035-os BibID:(cikkazonosító)600017 (WoS)000652520500001 (Scopus)85106199263
Első szerző:Töröcsik Dániel (bőrgyógyász)
Cím:Epidermal Growth Factor Modulates Palmitic Acid-Induced Inflammatory and Lipid Signaling Pathways in SZ95 Sebocytes / Dániel Törőcsik, Fruzsina Fazekas, Szilárd Póliska, Andrea Gregus, Eszter Anna Janka, Katalin Dull, Andrea Szegedi, Christos C. Zouboulis, Dóra Kovács
Dátum:2021
ISSN:1664-3224
Megjegyzések:Epidermal growth factor (EGF) acts as a paracrine and autocrine mediator of cell proliferation and differentiation in various types of epithelial cells, such as sebocytes, which produce the lipid-rich sebum to moisturize the skin. However, sebum lipids via direct contact and by penetrating through the epidermis may have regulatory roles on epidermal and dermal cells as well. As EGF receptor (EGFR) is expressed throughout the proliferating and the lipid-producing layers of sebaceous glands (SGs) in healthy and acne-involved skin, we investigated the effect of EGF on SZ95 sebocytes and how it may alter the changes induced by palmitic acid (PA), a major sebum component with bioactive roles. We found that EGF is not only a potent stimulator of sebocyte proliferation, but also induces the secretion of interleukin (IL)6 and down-regulates the expression of genes involved in steroid and retinoid metabolism. Importantly, when applied in combination with PA, the PA-induced lipid accumulation was decreased and the cells secreted increased IL6 levels. Functional clustering of the differentially regulated genes in SZ95 sebocytes treated with EGF, PA or co-treated with EGF+PA further confirmed that EGF may be a potent inducer of hyperproliferative/inflammatory pathways (IL1 signaling), an effect being more pronounced in the presence of PA. However, while a group of inflammatory genes was up-regulated significantly in EGF+PA co-treated sebocytes, PA treatment in the absence of EGF, regulated genes only related to cell homeostasis. Meta-analysis of the gene expression profiles of whole acne tissue samples and EGF- and EGF+PA ?treated SZ95 sebocytes showed that the EGF+PA co-activation of sebocytes may also have implications in disease. Altogether, our results reveal that PA-induced lipid accumulation and inflammation can be modulated by EGF in sebocytes, which also highlights the need for system biological approaches to better understand sebaceous (immuno)biology.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 12 (2021), p. 1-16. -
További szerzők:Fazekas Fruzsina (1993-) (biológus) Póliska Szilárd (1978-) (biológus) Gregus Andrea (1980-) (biológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Dull Katalin (1983-) (molekuláris biológus, genetikus) Szegedi Andrea (1964-) (bőrgyógyász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Kovács Dóra (1988-) (Biológus)
Pályázati támogatás:FK-132296
OTKA
K-128250
OTKA
Bolyai ösztöndíj
MTA
ÚNKP-20-5
Egyéb
GINOP-2.3.2-15-2016-00005
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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