Academic literature on the topic 'Oligogalacturonic Acid'

An efficient and inexpensive method for large-scale preparation of α-D-(1[Formula: see text]4)-oligogalacturonic acids (oligo-GalA), up to DP 5, from pectic acid is described. Pectic acid was digested with a commercially available pectinase to yield a mixture of oligo-GalA, which was effectively separated by a combination of low-pressure – size-exclusion chromatography based on ion-exchange chromatography to obtain pure oligo-GalA of DP 2-5. Key words: pectic acid, galacturonic acid, galabiose, galatriose, pectinase.

Pectate lyase (EC 4.2.2.2) catalyzes the cleavage of α-1,4-glycosidic bonds of pectin polymers, and it has potential uses in the textile industry. In this study, a novel pectate lyase belonging to polysaccharide lyase family 10 was screened from the secreted enzyme extract of Paenibacillus polymyxa KF-1 and identified by liquid chromatography-MS/MS. The gene was cloned from P. polymyxa KF-1 genomic DNA and expressed in Escherichia coli. The recombinant enzyme PpPel10a had a predicted Mr of 45.2 kDa and pI of 9.41. Using polygalacturonic acid (PGA) as substrate, the optimal conditions for PpPel10a reaction were determined to be 50 °C and pH 9.0, respectively. The Km, vmax and kcat values of PpPel10a with PGA as substrate were 0.12 g/L, 289 μmol/min/mg, and 202.3 s−1, respectively. Recombinant PpPel10a degraded citrus pectin, producing unsaturated mono- and oligogalacturonic acids. PpPel10a reduced the viscosity of PGA, and weight loss of ramie (Boehmeria nivea) fibers was observed after treatment with the enzyme alone (22.5%) or the enzyme in combination with alkali (26.3%). This enzyme has potential for use in plant fiber processing.

Les maladies cardiovasculaires (MCV) sont classées en tête de liste parmi les principales causes de décès dans le monde. La calcification de la paroi vasculaire entraîne diverses conséquences cardiovasculaires critiques et explique les taux de mortalité élevés chez les patients atteints de nombreuses maladies comme le diabète, l'athérosclérose et la maladie rénale chronique (IRC). VC est un processus actif avec des caractéristiques de la physiologie osseuse et il est régulé par des processus inductifs et inhibiteurs multifactoriels. Au cours du processus de calcification, les cellules musculaires lisses vasculaires (VSMC) subissent un processus ostéogénique actif pour devenir des cellules de type ostéoblaste et libérer des populations hétérogènes de Vésicules Extracellulaires (EV). Les VE agissent comme des foyers de nucléation pour la cristallisation grâce à leur interaction avec le collagène de type 1 (Col1) via les intégrines et leur teneur en protéines procalcifiantes soutient fortement la progression de la calcification. Parce que ces deux mécanismes sont cruciaux pour le développement de la VC, ils représentent finalement deux cibles thérapeutiques pour la régression de la VC. Notre objectif principal était d'identifier de nouvelles molécules naturelles ou synthétisées chimiquement pouvant inhiber la VC. Nous avons démontré la capacité d'un acide oligogalacturonique spécifique (DP8), extrait de graines de lin, à inhiber la calcification induite par Pi in vitro et ex vivo en diminuant l'expression des marqueurs ostéogéniques, masquant une répétition consensus des acides aminés trouvée dans Col1 (séquence: GFOGER) , et empêchant ainsi les VE de se lier. Nous avons également synthétisé chimiquement un peptide GFOGER et vérifié sa capacité à inhiber la calcification. Semblable à DP8, le peptide GFOGER a été capable d'inhiber la calcification induite par Pi in vitro et ex vivo en régulant à la baisse l'expression des marqueurs ostéogéniques et en modifiant la teneur en protéines des EV dérivés des VSMC. Par conséquent, nos travaux suggèrent deux nouvelles approches thérapeutiques pour la prévention de la CV
Cardiovascular diseases (CVDs) are classified on top of the list among different death leading causes in the world. Calcification of the vessel wall leads to various critical cardiovascular consequences and accounts for high mortality rates in patients with many diseases like diabetes, atherosclerosis and chronic kidney disease (CKD). VC is an active process with features of bone physiology and it is regulated by multifactorial inductive and inhibitory processes. During the calcification process, Vascular Smooth Muscle Cells (VSMCs) undergo active osteogenic process to become osteoblast-like cells and release heterogeneous populations of Extracellular Vesicles (EVs). EVs act as nucleating foci for crystallization through their interaction with type 1 collagen (Col1) via integrins and their procalcifying protein content strongly supports calcification progression. Because these two mechanisms are crucial for the development of VC, they eventually represent two therapeutic targets for VC regression. Our primary objective was to identify new natural or chemically synthesized molecules that can inhibit VC. We demonstrated the ability of a specific oligogalacturonic acid (DP8), extracted from flax seeds, to inhibit in vitro and ex-vivo Pi-induced calcification by diminishing osteogenic markers expression, masking a consensus amino acid repeat found in Col1 (sequence: GFOGER), and thus preventing EVs from binding. Also we chemically synthesized a GFOGER peptide and checked its ability to inhibit calcification. Similar to DP8, GFOGER peptide was able to inhibit in vitro and ex-vivo Pi-induced calcification by downregulating osteogenic markers expression and through modifying the protein content of VSMCs derived EVs. Therefore, our work suggests two novel therapeutic approaches for the prevention of VC