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Título

Myeloid GRK2 Regulates Obesity-Induced Endothelial Dysfunction by Modulating Inflammatory Responses in Perivascular Adipose Tissue

AutorGonzález-Amor, María; Vila-Bedmar, Rocío CSIC; Rodrigues-Diaz, Raquel; Moreno-Carriles, Rosa; Arcones, Alba C.; Cruces-Sande, Marta CSIC; Salaices, Mercedes; Mayor Méndez, Federico Jr.; Briones, Ana M.; Murga, Cristina CSIC ORCID
Palabras clavePerivascular adipose tissue (PVAT)
G protein-coupled receptor kinase 2 (GRK2)
Tumor necrosis factor- (TNF)
NADPH oxidase (Nox)
Endothelial dysfunction
Fecha de publicación4-oct-2020
EditorMultidisciplinary Digital Publishing Institute
CitaciónAntioxidants 9 (2020)
ResumenPerivascular adipose tissue (PVAT) is increasingly being regarded as an important endocrine organ that directly impacts vessel function, structure, and contractility in obesity-associated diseases. We uncover here a role for myeloid G protein-coupled receptor kinase 2 (GRK2) in the modulation of PVAT-dependent vasodilation responses. GRK2 expression positively correlates with myeloid- (CD68) and lymphoid-specific (CD3, CD4, and CD8) markers and with leptin in PVAT from patients with abdominal aortic aneurysms. Using mice hemizygous for GRK2 in the myeloid lineage (LysM-GRK2+/), we found that GRK2 deficiency in myeloid cells allows animals to preserve the endothelium-dependent acetylcholine or insulin-induced relaxation, which is otherwise impaired by PVAT, in arteries of animals fed a high fat diet (HFD). Downregulation of GRK2 in myeloid cells attenuates HFD-dependent infiltration of macrophages and T lymphocytes in PVAT, as well as the induction of tumor necrosis factor- (TNF) and NADPH oxidase (Nox)1 expression, whereas blocking TNF or Nox pathways by pharmacological means can rescue the impaired vasodilator responses to insulin in arteries with PVAT from HFD-fed animals. Our results suggest that myeloid GRK2 could be a potential therapeutic target in the development of endothelial dysfunction induced by PVAT in the context of obesity
Versión del editorhttp://dx.doi.org/10.3390/antiox9100953
URIhttp://hdl.handle.net/10261/237688
DOI10.3390/antiox9100953
Identificadoresdoi: 10.3390/antiox9100953
issn: 2076-3921
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