BMPER is upregulated in obesity and seems to have a role in pericardial adipose stem cells

Pericardial adipose tissue (PAT), a visceral fat depot enveloping the heart, is an active endocrine organ and a source of free fatty acids and inflammatory cytokines. As in other fat adult tissues, PAT contains a population of adipose stem cells; however, whether these cells and/or their environment...

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Detalles Bibliográficos
Autores: Pérez, Laura M., Lucas, Beatriz de, González Gálvez, Beatriz
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/104843
Acceso en línea:https://hdl.handle.net/20.500.14352/104843
Access Level:acceso abierto
Palabra clave:577.1
577.2
ASC
pericardial adipose tissue
cardiovascular disease
obesity
BMPER
Biología molecular (Farmacia)
Bioquímica (Farmacia)
32 Ciencias Médicas
Descripción
Sumario:Pericardial adipose tissue (PAT), a visceral fat depot enveloping the heart, is an active endocrine organ and a source of free fatty acids and inflammatory cytokines. As in other fat adult tissues, PAT contains a population of adipose stem cells; however, whether these cells and/or their environment play a role in physiopathology is unknown. We analyzed several stem cell‐related properties of pericardial adipose stem cells (PSCs) isolated from obese and ex‐obese mice. We also performed RNA‐sequencing to profile the transcriptional landscape of PSCs isolated from the different diet regimens. Finally, we tested whether these alterations impacted on the properties of cardiac mesoangioblasts isolated from the same mice. We found functional differences between PSCs depending on their source: specifically, PSCs from obese PSC (oPSC) and ex‐obese PSC (dPSC) mice showed alterations in apoptosis and migratory capacity when compared with lean, control PSCs, with increased apoptosis in oPSCs and blunted migratory capacity in oPSCs and dPSCs. This was accompanied by different gene expression profiles across the cell types, where we identified some genes altered in obese conditions, such as BMP endothelial cell precursor‐derived regulator (BMPER), an important regulator of BMP‐related signaling pathways for endothelial cell function. The importance of BMPER in PSCs was confirmed by loss‐ and gain‐of‐function studies. Finally, we found an altered production of BMPER and some important chemokines in cardiac mesoangioblasts in obese conditions. Our findings point to BMPER as a potential new regulator of PSC function and suggest that its dysregulation could be associated with obesity and may impact on cardiac cells.