000148848 001__ 148848
000148848 005__ 20250122151649.0
000148848 0247_ $$2doi$$a10.3390/ijms26010276
000148848 0248_ $$2sideral$$a142049
000148848 037__ $$aART-2024-142049
000148848 041__ $$aeng
000148848 100__ $$aDíez-Sainz, Ester
000148848 245__ $$aHuman miR-1 Stimulates Metabolic and Thermogenic-Related Genes in Adipocytes
000148848 260__ $$c2024
000148848 5060_ $$aAccess copy available to the general public$$fUnrestricted
000148848 5203_ $$aMicroRNAs play a pivotal role in the regulation of adipose tissue function and have emerged as promising therapeutic candidates for the management of obesity and associated comorbidities. Among them, miR-1 could be a potential biomarker for metabolic diseases and contribute to metabolic homeostasis. However, thorough research is required to fully elucidate the impact of miR-1 on human adipocyte thermogenesis and metabolism. This study aimed to explore the effect of miR-1 on human adipocyte browning, a process whose activation has been linked to obesity protection and counteraction. Human multipotent adipose-derived stem cells, hMADS cells, were differentiated into white and brown-like adipocytes and transfected with miR-1 mimics for gene expression and western blotting analyses. miR-1 inhibited the expression of its previously validated target PTK9/TWF1 and modulated the expression profile of key genes involved in thermogenesis and adipocyte browning (increased UCP1 at mRNA and protein level, increased CPT1M, decreased HIF3A), adipocyte differentiation and metabolism (decreased PLIN1, FASN, RXRA, PPARG, FABP4, MAPKAPK2), as well as genes related to the cytoskeleton (decreased ACTB) and extracellular matrix (decreased COL1A1). These findings suggest that miR-1 can modulate the expression of adipocyte human genes associated with thermogenesis and metabolism, which could hold value for eventual therapeutic potential in obesity.
000148848 536__ $$9info:eu-repo/grantAgreement/ES/MICINN /BFU2015-65937-R$$9info:eu-repo/grantAgreement/ES/MINECO/PID2022-141313OB-I00$$9info:eu-repo/grantAgreement/ES/MINECO/PID2022-141766OB-I00$$9info:eu-repo/grantAgreement/ES/MINECO/RTI2018-102205-B-I00
000148848 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000148848 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000148848 700__ $$aMilagro, Fermín I.
000148848 700__ $$aAranaz, Paula
000148848 700__ $$aRiezu-Boj, José I.
000148848 700__ $$aBatrow, Pierre-Louis
000148848 700__ $$aContu, Laura
000148848 700__ $$aGautier, Nadine
000148848 700__ $$aAmri, Ez-Zoubir
000148848 700__ $$aMothe-Satney, Isabelle
000148848 700__ $$0(orcid)0000-0002-1033-6152$$aLorente-Cebrián, Silvia$$uUniversidad de Zaragoza
000148848 7102_ $$11012$$2410$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Fisiología
000148848 773__ $$g26, 1 (2024), 276 [20 p.]$$pInt. j. mol. sci.$$tInternational Journal of Molecular Sciences$$x1661-6596
000148848 8564_ $$s2355099$$uhttps://zaguan.unizar.es/record/148848/files/texto_completo.pdf$$yVersión publicada
000148848 8564_ $$s2605055$$uhttps://zaguan.unizar.es/record/148848/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000148848 909CO $$ooai:zaguan.unizar.es:148848$$particulos$$pdriver
000148848 951__ $$a2025-01-22-14:46:33
000148848 980__ $$aARTICLE