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1. Imaging of Dysfunctional Elastogenesis in Atherosclerosis Using an Improved Gadolinium-Based Tetrameric MRI Probe Targeted to Tropoelastin

Author

Alkystis Phinikaridou, Giuseppe Digilio, Federico Capuana, Silvio Aime, René M. Botnar, Sergio Padovan, Eyad Almouazen, Begoña Lavin, Laurence Heinrich-Balard, Sara Lacerda, Yves Chevalier, Rachele Stefania, Department of Life Sciences and Systems Biology [University of Turin], University of Turin, School of Biomedical Engineering and Imaging Sciences, King's college London, King‘s College London, Molecular Biotechnology Center, Università degli studi di Torino (UNITO), Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Université d'Orléans (UO), Laboratoire d'automatique, de génie des procédés et de génie pharmaceutique (LAGEPP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Supérieure Chimie Physique Électronique de Lyon-Centre National de la Recherche Scientifique (CNRS), Matériaux, ingénierie et science [Villeurbanne] (MATEIS), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS), Pontificia Universidad Católica de Chile: Santiago, Región Metropolitana, CL, IRCCS SDN Napoli, Università degli Studi del Piemonte Orientale, Dipartimento di Scienze e Innovazione Tecnologica, Alessandria, Italy, Centre de biophysique moléculaire (CBM), Université d'Orléans (UO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC), Pontificia Universidad Católica de Chile (UC), Università degli Studi del Piemonte Orientale - Amedeo Avogadro (UPO), Università degli studi di Torino = University of Turin (UNITO), Université d'Orléans (UO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Université de Lyon-École Supérieure de Chimie Physique Électronique de Lyon (CPE)-Centre National de la Recherche Scientifique (CNRS), Martins Vasco de Lacerda, Sara, and Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Contrast enhancement, MRI contrast agent, Gadolinium, chemistry.chemical_element, Contrast Media, Peptide, 030204 cardiovascular system & hematology, 01 natural sciences, Article, 03 medical and health sciences, Mice, 0302 clinical medicine, Time windows, Tropoelastin, [CHIM] Chemical Sciences, Drug Discovery, [CHIM]Chemical Sciences, Animals, ComputingMilieux_MISCELLANEOUS, chemistry.chemical_classification, Mice, Knockout, biology, integumentary system, Molecular Structure, 010405 organic chemistry, Chemistry, [CHIM.MATE]Chemical Sciences/Material chemistry, Surface Plasmon Resonance, Atherosclerosis, Magnetic Resonance Imaging, 0104 chemical sciences, Elastin, Mice, Inbred C57BL, Disease Models, Animal, Biophysics, biology.protein, Molecular Medicine, [SDV.IB]Life Sciences [q-bio]/Bioengineering, Molecular imaging
Abstract

International audience; Dysfunctional elastin turnover plays a major role in the progression of atherosclerotic plaques. Failure of tropoelastin cross-linking into mature elastin leads to the accumulation of tropoelastin within the growing plaque, increasing its instability. Here we present Gd4-TESMA, an MRI contrast agent specifically designed for molecular imaging of tropoelastin within plaques. Gd4-TESMA is a tetrameric probe composed of a tropoelastin-binding peptide (the VVGS-peptide) conjugated with four Gd(III)-DOTA-monoamide chelates. It shows a relaxivity per molecule of 34.0 ± 0.8 mM-1 s-1 (20 MHz, 298 K, pH 7.2), a good binding affinity to tropoelastin (KD = 41 ± 12 μM), and a serum half-life longer than 2 h. Gd4-TESMA accumulates specifically in atherosclerotic plaques in the ApoE-/- murine model of plaque progression, with 2 h persistence of contrast enhancement. As compared to the monomeric counterpart (Gd-TESMA), the tetrameric Gd4-TESMA probe shows a clear advantage regarding both sensitivity and imaging time window, allowing for a better characterization of atherosclerotic plaques.

Published
2021
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2. MISSENSE MUTATIONS IN THE AFG3L2 PROTEOLYTIC DOMAIN ACCOUNT FOR ~1.5% OF EUROPEAN AUTOSOMAL DOMINANT CEREBELLAR ATAXIAS

Author

Luisa Pugliese, Marcello Nobili, Corrado Assalto, Russell L. Margolis, Pascale Ribai, Nicola Migone, Claudia Cagnoli, Sylvie Forlani, Patrizia Pappi, Giovanni Stevanin, Alessandro Brussino, Isabelle Leber, Alexis Brice, Susan E. Holmes, Sergio Padovan, Marco Barberis, Alexandra Durr, Alfredo Brusco, Cécile Zaros, Cecilia Mancini, Genetics Biology and Biochemistry, University of Turin, Polytech'Paris-UPMC, Université Pierre et Marie Curie - Paris 6 (UPMC), Johns Hopkins University School of Medicine [Baltimore], Division of Neurology, Martini Hospital, CNR Istituto Di Biostrutture E Bioimmagini (IBB-CNR), Consiglio Nazionale delle Ricerche [Torino] (CNR), SAFAN bioinformatics, Neurologie et thérapeutique expérimentale, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR70-Université Pierre et Marie Curie - Paris 6 (UPMC), Department of Genetics Biology and Biochemistry, Università degli studi di Torino = University of Turin (UNITO), CNR Istituto di biostrutture e bioimmagini [ Napoli] (CNR | IBB), National Research Council of Italy | Consiglio Nazionale delle Ricerche (CNR), and Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR70-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Adult, Male, Models, Molecular, Adolescent, Cerebellar Ataxia, Mutation, Missense, Biology, medicine.disease_cause, White People, 03 medical and health sciences, Exon, Young Adult, 0302 clinical medicine, Autosomal dominant cerebellar ataxia, ATP-Dependent Proteases, Genetics, medicine, Prevalence, Missense mutation, Humans, Spinocerebellar Ataxias, Child, Gene, Genetics (clinical), 030304 developmental biology, Aged, Genes, Dominant, Spinocerebellar Degenerations, 0303 health sciences, Mutation, Cerebellar ataxia, Point mutation, Computational Biology, Infant, Life Sciences, Middle Aged, medicine.disease, Molecular biology, 3. Good health, Pedigree, Europe, Child, Preschool, Spinocerebellar ataxia, ATPases Associated with Diverse Cellular Activities, Female, medicine.symptom, 030217 neurology & neurosurgery
Abstract

Spinocerebellar ataxia type 28 is an autosomal dominant form of cerebellar ataxia (ADCA) caused by mutations in AFG3L2, a gene that encodes a subunit of the mitochondrial m-AAA protease. We screened 366 primarily Caucasian ADCA families, negative for the most common triplet expansions, for point mutations in AFG3L2 using DHPLC. Whole-gene deletions were excluded in 300 of the patients, and duplications were excluded in 129 patients. We found six missense mutations in nine unrelated index cases (9/366, 2.6%): c.1961C>T (p.Thr654Ile) in exon 15, c.1996A>G (p.Met666Val), c.1997T>G (p.Met666Arg), c.1997T>C (p.Met666Thr), c.2011G>A (p.Gly671Arg), and c.2012G>A (p.Gly671Glu) in exon 16. All mutated amino acids were located in the C-terminal proteolytic domain. In available cases, we demonstrated the mutations segregated with the disease. Mutated amino acids are highly conserved, and bioinformatic analysis indicates the substitutions are likely deleterious. This investigation demonstrates that SCA28 accounts for ∼3% of ADCA Caucasian cases negative for triplet expansions and, in extenso, to ∼1.5% of all ADCA. We further confirm both the involvement of AFG3L2 gene in SCA28 and the presence of a mutational hotspot in exons 15–16. Screening for SCA28, is warranted in patients who test negative for more common SCAs and present with a slowly progressive cerebellar ataxia accompanied by oculomotor signs. Hum Mutat 31:1–8, 2010. © 2010 Wiley-Liss, Inc.

Published
2010
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