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Nicolas-Avila, J. A.

Publications and source records attributed to Nicolas-Avila, J. A..

2 recordsLinked to original sources

HDL-associated phosphatidylserine blunts myeloid activation and protects from atherosclerosis

Background and aimsLipids play a critical role in atherosclerosis. Low-density lipoprotein (LDL)-cholesterol and certain lipid classes like sphingomyelins are associated with inflammation and poor cardiovascular outcomes. Phosphatidylserine (PS), on the other hand, is a negatively charged anti-inflammatory phospholipid class involved in efferocytosis. In this study, we sought to investigate its anti-atherosclerotic properties through a combination of complementary human lipidomics analyses, in vitro assays and in vivo experiments in Apoe-/- mice. MethodsHuman lipidomics studies were performed on the 300OB cohort comprising 300 obese and overweight individuals at risk of cardiovascular disease. In vitro assays were carried out using human monocytes and macrophages, and in vivo experiments included histopathological, immunophenotyping and single-cell transcriptomic analyses. ResultsIn humans, we identified PS as an anti-inflammatory and atheroprotective biomarker. Hence, we developed a high-density lipoprotein (HDL)-like formulation enriched in PS to exploit its properties in a targeted fashion in mice. In vitro, this formulation potently inhibited inflammatory cytokine production on human myeloid cells. Our in-depth in vivo experiments provided evidence of the formulations potent plaque-stabilizing and anti-inflammatory actions. These effects were mediated by a shift in the monocyte/macrophage compartment toward homeostatic/repairing phenotypes. ConclusionsCollectively, our results demonstrate that HDL-associated PS potently suppresses inflammation and atheroprogression, and holds promise as a viable approach to improve immunomodulatory therapies.

immunology↗

Vascular HIF2 signaling prevents cardiomegaly, alveolar congestion and capillary remodeling during chronic hypoxia

Hypoxia is associated with the onset of cardiovascular diseases including cardiac hypertrophy and pulmonary arterial hypertension (PAH). Endothelial HIF2 signaling mediates pulmonary arterial remodeling and subsequent right ventricular systolic pressure (RVSP) elevation during chronic hypoxia, encouraging novel therapeutic opportunities for PAH based on specific HIF2 inhibitors. Nevertheless, HIF2 relevance beyond the pulmonary endothelium or in the cardiac adaptation to hypoxia remains elusive. Wilms tumor 1 lineage contributes to heart and lung vascular compartments including pericytes, endothelial and smooth muscle cells. Here we describe the response to chronic hypoxia of a novel HIF2 mutant mouse model in the Wt1 lineage (Hif2/Wt1 cKO). Hif2/Wt1 cKO is protected against pulmonary remodeling and increased RVSP induced by hypoxia, but displays alveolar congestion, inflammation and hemorrhages associated with microvascular instability. Furthermore, lack of HIF2 in the Wt1 lineage leads to cardiomegaly, capillary remodeling, right and left ventricular hypertrophy, systolic dysfunction and left ventricular dilation, suggesting pulmonary-independent cardiac direct roles of HIF2 in hypoxia. These structural defects are partially restored upon reoxygenation, while functional parameters remain altered. Our results suggest that cardiopulmonary HIF2 signaling prevents excessive vascular proliferation during chronic hypoxia and define novel protective roles of HIF2 to warrant stable microvasculature and organ function.

pathology↗