Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms

• DOI: 10.1161/atvbaha.117.309513
• Publication Date: 2017-05-19T01:00:17Z
• Authors: Ahmed Hodroge; Eric Trécherel; Marjorie Cornu; Walaa Darwiche; Ali Mansour; Katia Ait-Mohand; Thomas Verissimo; Cathy Gomila; Carole Schembri; Sophie Da Nascimento; Redouan Elboutach...; Agnès Boullier; Emmanuel Lorne; Josiane Courtois; Emmanuel Petit; Sylvestre Toumieux; José Kovensky; Pascal Sonnet; Ziad A. Massy; Saïd Kamel; Claire Rossi; Jérôme Ausseil
• Keywords: matrix Gla protein

Objective— Cardiovascular diseases constitute the leading cause of mortality worldwide. Calcification vessel wall is associated with cardiovascular morbidity and in patients having many diseases, including diabetes mellitus, atherosclerosis, chronic kidney disease. Vascular calcification actively regulated by inductive inhibitory mechanisms (including vascular smooth muscle cell adaptation) results from an active osteogenic process. During process, extracellular vesicles (also known as matrix vesicles) released cells interact type I collagen then act nucleating foci for calcium crystallization. Our primary objective was to identify new, natural molecules that inhibit Approach Results— We have found oligogalacturonic acids (obtained acid hydrolysis polygalacturonic acid) reduce vitro inorganic phosphate–induced 80% isolated rat aortic rings 50%. A specific a degree polymerization 8 (DP8) expression markers and, thus, prevent conversion into osteoblast-like cells. also evidenced biochemical immunofluorescence assays direct interaction between via GFOGER sequence (where single letter amino nomenclature used, O=hydroxyproline) thought be involved interactions several pairs integrins. Conclusions— DP8 inhibits development mainly inhibition marker but partly masking sequence—thereby, preventing binding collagen.