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Eur Heart J ; 36(13): 806-16, 2015 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-25368203

RESUMO

AIMS: High-fat diet-induced obesity (DIO) is a major contributor to type II diabetes and micro- and macro-vascular complications leading to peripheral vascular disease (PVD). Metabolic abnormalities of induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) from obese individuals could potentially limit their therapeutic efficacy for PVD. The aim of this study was to compare the function of iPSC-ECs from normal and DIO mice using comprehensive in vitro and in vivo assays. METHODS AND RESULTS: Six-week-old C57Bl/6 mice were fed with a normal or high-fat diet. At 24 weeks, iPSCs were generated from tail tip fibroblasts and differentiated into iPSC-ECs using a directed monolayer approach. In vitro functional analysis revealed that iPSC-ECs from DIO mice had significantly decreased capacity to form capillary-like networks, diminished migration, and lower proliferation. Microarray and ELISA confirmed elevated apoptotic, inflammatory, and oxidative stress pathways in DIO iPSC-ECs. Following hindlimb ischaemia, mice receiving intramuscular injections of DIO iPSC-ECs had significantly decreased reperfusion compared with mice injected with control healthy iPSC-ECs. Hindlimb sections revealed increased muscle atrophy and presence of inflammatory cells in mice receiving DIO iPSC-ECs. When pravastatin was co-administered to mice receiving DIO iPSC-ECs, a significant increase in reperfusion was observed; however, this beneficial effect was blunted by co-administration of the nitric oxide synthase inhibitor, N(ω)-nitro-l-arginine methyl ester. CONCLUSION: This is the first study to provide evidence that iPSC-ECs from DIO mice exhibit signs of endothelial dysfunction and have suboptimal efficacy following transplantation in a hindlimb ischaemia model. These findings may have important implications for future treatment of PVD using iPSC-ECs in the obese population.


Assuntos
Células Endoteliais/fisiologia , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Células-Tronco Pluripotentes Induzidas/fisiologia , Óxido Nítrico/fisiologia , Obesidade/fisiopatologia , Pravastatina/farmacologia , Análise de Variância , Animais , Apoptose/fisiologia , Diferenciação Celular , Dieta Hiperlipídica , Inibidores Enzimáticos/farmacologia , Fibroblastos/fisiologia , Membro Posterior/irrigação sanguínea , Injeções Intramusculares , Isquemia/fisiopatologia , Isquemia/prevenção & controle , Camundongos Endogâmicos C57BL , Músculo Esquelético , Doenças Musculares/prevenção & controle , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico Sintase Tipo III/metabolismo , Estresse Oxidativo/fisiologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Distribuição Aleatória , Traumatismo por Reperfusão/fisiopatologia , Transdução de Sinais
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