Showing papers by "José Luis Sánchez-Quesada published in 2017"
TL;DR: It was confirmed that rHDL-rApoJ accumulated in the cranial region, especially in old transgenic mice presenting a high cerebral Aβ load, which may be potentially considered as a therapeutic option for β-amyloid-related pathologies.
Abstract: Cerebral β-amyloidosis is a major feature of Alzheimer's disease (AD), characterized by the accumulation of β-amyloid protein (Aβ) in the brain. Several studies have implicated lipid/lipoprotein metabolism in the regulation of β-amyloidosis. In this regard, HDL (High Density Lipoprotein)-based therapies could ameliorate pathological features associated with AD. As apolipoprotein J (ApoJ) is a natural chaperone that interacts with Aβ, avoiding its aggregation and toxicity, in this study we propose to prepare reconstituted rHDL-rApoJ nanoparticles by assembling phospholipids with recombinant human ApoJ (rApoJ). Hence, rHDL particles were prepared using the cholate dialysis method and characterized by N-PAGE, dynamic light scattering, circular dichroism and electron transmission microscopy. The preparation of rHDL particles showed two-sized populations with discoidal shape. Functionally, rHDL-rApoJ maintained the ability to prevent the Aβ fibrillization and mediated a higher cholesterol efflux from cultured macrophages. Fluorescently-labelled rHDL-rApoJ nanoparticles were intravenously administrated in mice and their distribution over time was determined using an IVIS Xenogen® imager. It was confirmed that rHDL-rApoJ accumulated in the cranial region, especially in old transgenic mice presenting a high cerebral Aβ load. In conclusion, we have standardized a reproducible protocol to produce rHDL-rApoJ nanoparticles, which may be potentially considered as a therapeutic option for β-amyloid-related pathologies.
27 citations
TL;DR: The findings show an imbalance in the pro- and anti-inflammatory effects of lipoproteins from T2DM patients, particularly in PC-T2DM.
14 citations
TL;DR: In this article, the HDL lipid composition influences amyloid deposition by apoA-I and related proteins, and the results suggest that decreasing plasma levels of triglycerides will shift the dynamic equilibrium from the lipidpoor/free (labile) to the HDL-bound (protected) apolipoprotein state, thereby decreasing the generation of the protein precursor of amyloids.
12 citations
1 citations
TL;DR: The available evidence supports the relationship between hypovitaminosis D and metabolic syndrome components, including atherogenic dyslipidaemia, but the causal relationship is yet to be established.
Abstract: We appreciate the interest of Katsiki et al. [1] in our review entitled The Association of hypovitaminosis D and metabolic syndrome: current understanding, published in Clinical Lipidology [2].We c...
1 citations