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001-es BibID:	BIBFORM079713
035-os BibID:	(WoS)000486972404107
Első szerző:	Arianti, Rini (biokémikus)
Cím:	Identification of unique molecular signature ofbrowning in human primary adipocytes fromdeep and subcutaneous neck fat / Arianti Rini, Shaw Abhirup, Vámos Attila, Bartáné Tóth Beáta, Győry Ferenc, Póliska Szilárd, Kristóf Endre Károly, Fésüs László
Dátum:	2019
ISSN:	2211-5463
Megjegyzések:	There are two types of thermogenic adipocytes, classical brown and beige (BAT) which are UCP1-positive dissipating energy as heat. BAT markers have been well studied in rodents but detailed molecular studies are still lacking in humans where BAT is interspersed at several sites and may serve as a target of anti-obesity therapies. Our study aims to identify the unique signature of browning in human primary adipocytes from the different anatomical location by analyzing global gene expression patterns. Preadipocytes were obtained from subcutaneous (SC) and deep neck (DN) and differentiated to white and brown adipocytes. We analyzed differential gene expressions by total RNA sequencing, molecular pathways by KEGG Mapper, genetic constraint by ExAC and verified several genes of interest associated with adipocytes browning. We identified 37 genes which are closely clustered to UCP1. Out of those 13 genes have been already described to play a role in thermogenesis (CIDEA, CKMT1A/B), while the roles of the others are still unclear (ANO5, FAM151a). Several pathways were represented, such as retinoic acid biosynthesis which was upregulated (CPT1, CYP261B), while extracellular matrix organization pathways were among the downregulated ones (COL, ITGF). Mitochondrial creatine kinases, CKMT1a/b, are reported to play role in UCP1-independent thermogenesis; UCP1 and CKMT1a were expressed higher in DN, as compared to SC adipocytes and this was verified by RT-qPCR. Several transporters were expressed higher in DN, such as transporter of amino acids (SLC7A10), glutamate (SLC25A18) and pyruvate (SLC16A7). Our data proves that progenitors from DN fat can be differentiated to browning adipocytes at a greater extent than SC ones. We have started to investigate revealed molecular elements not linked yet to browning by deleting, inhibiting or overexpressing them.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok poszter folyóiratcikk
Megjelenés:	FEBS Open Bio. - 9 : S1 (2019), p. 289-290. -
További szerzők:	Shaw, Abhirup (1992-) Vámos Attila (1991-) (gyógyszer-biotechnológus) Bartáné Tóth Beáta (1970-) (molekuláris biológus) Győry Ferenc (1969-) (kardiológus) Póliska Szilárd (1978-) (biológus) Kristóf Endre (1987-) (általános orvos) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00006 GINOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM084780
035-os BibID:	(cikkazonosító)987 (WOS)000535559500198 (Scopus)85083871362
Első szerző:	Bartáné Tóth Beáta (molekuláris biológus)
Cím:	FTO intronic SNP strongly influences human neck adipocyte browning determined by tissue and PPARγ specific regulation : a transcriptome analysis / Bartáné Tóth Beáta, Arianti Rini, Shaw Abhirup, Vámos Attila, Veréb Zoltán, Póliska Szilárd, Győry Ferenc, Bacsó Zsolt, Fésüs László, Kristóf Endre Károly
Dátum:	2020
ISSN:	2073-4409
Megjegyzések:	Brown adipocytes, abundant in deep-neck (DN) area in humans, are thermogenic with anti-obesity potential. FTO pro-obesity rs1421085 T-to-C SNP shifts differentiation program towards white adipocytes in subcutaneous fat. Human adipose-derived stromal cells were obtained from subcutaneous neck (SC) and DN fat of 9 donors, of which 3-3 carried risk-free (T/T), heterozygous or obesity-risk (C/C) FTO genotypes. They were differentiated to white and brown (long-term PPAR? stimulation) adipocytes, then global RNA sequencing was performed and differentially expressed genes (DEGs) were compared. DN and SC progenitors had similar adipocyte differentiation potential but differed in DEGs. DN adipocytes displayed higher browning features according to ProFAT or BATLAS scores and characteristic DEG patterns revealing associated pathways which were highly expressed (thermogenesis, interferon, cytokine, retinoic acid, with UCP1 and BMP4 as prominent network stabilizers) or downregulated (particularly extracellular matrix remodelling) compared to SC ones. Part of DEGs in either DN or SC browning was PPAR?-dependent. Presence of the FTO obesity-risk allele suppressed the expression of mitochondrial and thermogenesis genes with a striking resemblance between affected pathways and those appearing in ProFAT and BATLAS, underlining the importance of metabolic and mitochondrial pathways in thermogenesis. Among overlapping regulatory influences which determine browning and thermogenic potential of neck adipocytes, FTO genetic background has a so far not recognized prominence.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk adipocyte browning differential gene expression patterns deep-neck PPARg FTO obesity-risk allele
Megjelenés:	Cells. - 9 : 4 (2020), p. 1-25. -
További szerzők:	Arianti, Rini (1991-) (biokémikus) Shaw, Abhirup (1992-) Vámos Attila (1991-) (gyógyszer-biotechnológus) Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Póliska Szilárd (1978-) (biológus) Győry Ferenc (1969-) (kardiológus) Bacsó Zsolt (1963-) (biofizikus) Fésüs László (1947-) (orvos biokémikus) Kristóf Endre (1987-) (általános orvos)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00006 GINOP FIKP_20428-3_2018_FELITSTRAT FIKP FK131424 OTKA K129139 OTKA EFOP-3.6.3-VEKOP-16-2017-00009 EFOP ÚNKP-19-4-DE-42 Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM077512
Első szerző:	Kristóf Endre (általános orvos)
Cím:	Interleukin-6 released from differentiating human beige adipocytes improves browning / Endre Kristóf, Ágnes Klusóczki, Roland Veress, Abhirup Shaw, Zsolt Sándor Combi, Klára Varga, Ferenc Győry, Zoltán Balajthy, Péter Bai, Zsolt Bacso, László Fésüs
Dátum:	2019
ISSN:	0014-4827
Megjegyzések:	Brown and beige adipocytes contribute significantly to the regulation of whole body energy expenditure and systemic metabolic homeostasis not exclusively by thermogenesis through mitochondrial uncoupling. Several studies have provided evidence in rodents that brown and beige adipocytes produce a set of adipokines ("batokines") which regulate local tissue homeostasis and have beneficial effects on physiological functions of the entire body. We observed elevated secretion of Interleukin (IL)-6, IL-8 and monocyte chemoattractant protein (MCP)-1, but not tumor necrosis factor alpha (TNFα) or IL-1β pro-inflammatory cytokines, by ex vivo differentiating human beige adipocytes (induced by either PPARγ agonist or irisin) compared to white. Higher levels of IL-6, IL-8 and MCP-1 were released from human deep neck adipose tissue biopsies (enriched in browning cells) than from subcutaneous ones. IL-6 was produced in a sustained manner and mostly by the adipocytes and not by the undifferentiated progenitors. Continuous blocking of IL-6 receptor by specific antibody during beige differentiation resulted in downregulation of brown marker genes and increased morphological changes that are characteristic of white adipocytes. The data suggest that beige adipocytes adjust their production of IL-6 to reach an optimal level for differentiation in the medium enhancing browning in an autocrine manner.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Experimental Cell Research. - 377 : 1-2 (2019), p. 47-55. -
További szerzők:	Klusóczki Ágnes (1991-) (biotechnológus) Veress Roland (1992-) (molekuláris biológus) Shaw, Abhirup (1992-) Combi Zsolt Varga Klára Győry Ferenc (1969-) (kardiológus) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus) Bai Péter (1976-) (biokémikus) Bacsó Zsolt (1963-) (biofizikus) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00006 GINOP OTKA-NK105046 OTKA OTKA-K123975 OTKA ÚNKP-18-4 ÚNKP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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