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by Keyword: pathogenesis

Azagra, Marc, Pose, Elisa, Chiara, Francesco, Perez, Martina, Avitabile, Emma, Servitja, Joan‐Marc, Brugnara, Laura, Ramon‐Azcón, Javier, Marco‐Rius, Irene, (2022). Ammonium quantification (AQua) in human plasma by 1 H‐NMR for staging of liver fibrosis in alcohol‐related liver disease and non‐alcoholic fatty liver disease Nmr In Biomedicine 35, e4745

Gouveia, Virgínia M., Rizzello, Loris, Vidal, Bruno, Nunes, Claudia, Poma, Alessandro, Lopez?Vasquez, Ciro, Scarpa, Edoardo, Brandner, Sebastian, Oliveira, António, Fonseca, João E., Reis, Salette, Battaglia, Giuseppe, (2022). Targeting Macrophages and Synoviocytes Intracellular Milieu to Augment Anti-Inflammatory Drug Potency Advanced Therapeutics 5, 2100167

Bertran, Oscar, Martí, Didac, Torras, Juan, Turon, Pau, Alemán, Carlos, (2022). Computer simulations on oxidative stress-induced reactions in SARS-CoV-2 spike glycoprotein: a multi-scale approach Molecular Diversity ,

Abstract Oxidative stress, which occurs when an organism is exposed to an adverse stimulus that results in a misbalance of antioxidant and pro-oxidants species, is the common denominator of diseases considered as a risk factor for SARS-CoV-2 lethality. Indeed, reactive oxygen species caused by oxidative stress have been related to many virus pathogenicity. In this work, simulations have been performed on the receptor binding domain of SARS-CoV-2 spike glycoprotein to study what residues are more susceptible to be attacked by ·OH, which is one of the most reactive radicals associated to oxidative stress. The results indicate that isoleucine (ILE) probably plays a crucial role in modification processes driven by radicals. Accordingly, QM/MM-MD simulations have been conducted to study both the ·OH-mediated hydrogen abstraction of ILE residues and the induced modification of the resulting ILE radical through hydroxylation or nitrosylation reactions. All in all, in silico studies show the importance of the chemical environment triggered by oxidative stress on the modifications of the virus, which is expected to help for foreseeing the identification or development of antioxidants as therapeutic drugs. Graphic abstract

JTD Keywords: atom abstraction, damage, density functionals, hydrogen abstraction, isoleucine, molecular dynamics, pathogenesis, protein, reactive oxygen species, receptor binding domain, residues, spike protein, Amino-acids, Hydrogen abstraction, Isoleucine, Molecular dynamics, Reactive oxygen species, Receptor binding domain, Spike protein


Tura-Ceide O, Smolders VFED, Aventin N, Morén C, Guitart-Mampel M, Blanco I, Piccari L, Osorio J, Rodríguez C, Rigol M, Solanes N, Malandrino A, Kurakula K, Goumans MJ, Quax PHA, Peinado VI, Castellà M, Barberà JA, (2021). Derivation and characterisation of endothelial cells from patients with chronic thromboembolic pulmonary hypertension Scientific Reports 11, 18797-18797

Pulmonary endarterectomy (PEA) resected material offers a unique opportunity to develop an in vitro endothelial cell model of chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to comprehensively analyze the endothelial function, molecular signature, and mitochondrial profile of CTEPH-derived endothelial cells to better understand the pathophysiological mechanisms of endothelial dysfunction behind CTEPH, and to identify potential novel targets for the prevention and treatment of the disease. Isolated cells from specimens obtained at PEA (CTEPH-EC), were characterized based on morphology, phenotype, and functional analyses (in vitro and in vivo tubule formation, proliferation, apoptosis, and migration). Mitochondrial content, morphology, and dynamics, as well as high-resolution respirometry and oxidative stress, were also studied. CTEPH-EC displayed a hyperproliferative phenotype with an increase expression of adhesion molecules and a decreased apoptosis, eNOS activity, migration capacity and reduced angiogenic capacity in vitro and in vivo compared to healthy endothelial cells. CTEPH-EC presented altered mitochondrial dynamics, increased mitochondrial respiration and an unbalanced production of reactive oxygen species and antioxidants. Our study is the foremost comprehensive investigation of CTEPH-EC. Modulation of redox, mitochondrial homeostasis and adhesion molecule overexpression arise as novel targets and biomarkers in CTEPH.

JTD Keywords: angiogenesis, cd31, dysfunction, expression, pathogenesis, thrombus, C-reactive protein