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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
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2.

001-es BibID:BIBFORM102713
Első szerző:Shaw, Abhirup
Cím:Irisin stimulates the release of CXCL1 via upregulation of NFkB pathway from human neck derived differentiating adipocytes / Shaw Abhirup, B. Tóth Beáta, Győry Ferenc, Fésüs László, Kristóf Endre
Dátum:2022
ISSN:2211-5463
Megjegyzések:Obesity is at present a global epidemic. Brown and beige adipocytes function in utilizing excess fat to produce heat (thermogenesis), thereby counteracting obesity. Recent studies in rodents and humans indicated that these adipocytes also release cytokines, which may play a vital role in maintaining whole body energy homeostasis. Irisin is primarily released by myocytes during exercise and functions as a polypeptide regulator of beige adipocytes. We intended to characterize the effect of irisin on differentiating adipocytes derived from human subcutaneous neck (SC) and deep neck (DN) adipose tissue depots. Preadipocytes were isolated from SC and DN biopsies of the same donor, differentiated to adipocytes in the presence or absence of irisin. Global gene expression analysis was performed on nine independent donors. Irisin could not upregulate characteristic thermogenic genes, but upregulated genes related to several cytokines. Out of them,CXCL1 (the highest upregulated) was found to be released throughout the differentiation period, predominantly by SC and DN differentiated adipocytes. DN tissue biopsies showed a significant release of CXCL1 upon 24 hours irisin treatment. Geneexpression data indicated upregulation of the NFkB pathway upon irisin treatment, which was validated by an increase of p50 and decrease of IkBa protein level, respectively. Continuous blocking of the NFkB pathway by SN50 (cell permeable inhibitorof NFkB nuclear translocation) significantly reduced the release of CXCL1. The released CXCL1 exerted a positive effect on the adhesion capability of endothelial cells. Together, our findings demonstrate that irisin stimulates the release of a novel adipokine, CXCL1, via upregulation of NFkB pathway in human neck area derived differentiating adipocytes, which plays an important role in improving tissue vascularization (Previously published in:Shaw A et al. (2021) Front Cell Dev Biol 9:737872).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:FEBS Open Bio. - 12 : S1 (2022), p. 208. -
További szerzők:Bartáné Tóth Beáta (1970-) (molekuláris biológus) Győry Ferenc (1964-) (sebész) Fésüs László (1947-) (orvos biokémikus) Kristóf Endre (1987-) (általános orvos)
Pályázati támogatás:FK131424
OTKA
GINOP-2.3.2-15-2016-00006
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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