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      Excessive Methionine Supplementation Exacerbates the Development of Abdominal Aortic Aneurysm in Rats

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          Abstract

          Objective: The relationship between methionine (Met) and abdominal aortic aneurysm (AAA) has been previously demonstrated, but the mechanisms controlling this association remain unclear. This study investigated the potential contribution of hypermethioninemia (HMet) to the development of AAA. Methods: A model of AAA was induced by intraluminal porcine pancreatic elastase (PPE) infusion in 60 male Sprague-Dawley rats divided into 4 groups ( n = 15 per group). Met was supplied by intragastric administration (1 g/kg body weight/day) from 1 week before surgery until 4 weeks after surgery. The aortic diameter was measured by ultrasound. Aortas were collected 4 weeks after surgery and subjected to biochemical analysis, histological assays, and transmission electron microscopy. Results: After 5 weeks of Met supplementation, HMet increased the dilation ratio of the HMet + PPE group, and hyperhomocysteinemia was also induced in HMet and HMet + PPE rats. Increased matrix metalloproteinase-2 (MMP-2), osteopontin, and interleukin-6 expression was detected in HMet + PPE rats. Furthermore, increased autophagy was detected in the HMet + PPE group. Conclusion: This study demonstrates that HMet may exacerbate the formation of AAA due to the increased dilation ratio partially via enhancing MMP-2 and inflammatory responses.

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          Homocysteine metabolism.

          J Selhub (1999)
          Homocysteine is a sulfur amino acid whose metabolism stands at the intersection of two pathways: remethylation to methionine, which requires folate and vitamin B12 (or betaine in an alternative reaction); and transsulfuration to cystathionine, which requires pyridoxal-5'-phosphate. The two pathways are coordinated by S-adenosylmethionine, which acts as an allosteric inhibitor of the methylenetetrahydrofolate reductase reaction and as an activator of cystathionine beta-synthase. Hyperhomocysteinemia, a condition that recent epidemiological studies have shown to be associated with increased risk of vascular disease, arises from disrupted homocysteine metabolism. Severe hyperhomocysteinemia is due to rare genetic defects resulting in deficiencies in cystathionine beta synthase, methylenetetrahydrofolate reductase, or in enzymes involved in methyl-B12 synthesis and homocysteine methylation. Mild hyperhomocysteinemia seen in fasting conditions is due to mild impairment in the methylation pathway (i.e. folate or B12 deficiencies or methylenetetrahydrofolate reductase thermolability). Post-methionine-load hyperhomocysteinemia may be due to heterozygous cystathionine beta-synthase defect or B6 deficiency. Early studies with nonphysiological high homocysteine levels showed a variety of deleterious effects on endothelial or smooth muscle cells in culture. More recent studies with human beings and animals with mild hyperhomocysteinemia provided encouraging results in the attempt to understand the mechanism that underlies this relationship between mild elevations of plasma homocysteine and vascular disease. The studies with animal models indicated the possibility that the effect of elevated homocysteine is multifactorial, affecting both the vascular wall structure and the blood coagulation system.
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            Monocytes and macrophages in abdominal aortic aneurysm

            Juliette Raffort, Fabien Lareyre, Marc Clement … (2017)
            Inflammatory processes have a crucial role in abdominal aortic aneurysm and aortic wall remodelling. This Review focuses on the involvement of monocytes and macrophages, summarizing current knowledge on their origin and the roles of distinct monocyte and macrophage subsets in AAA development and complications, and highlighting potential translational applications targeting monocytes and macrophages.
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              Homocysteine-Induced Endothelial Dysfunction

              Wai Lai, Ming Yin Kan (2015)
              This review discussed and in particular emphasis the potential cellular pathways and the biological processes involved that lead to homocysteine-induced endothelial dysfunction, in particular in the impaired endothelial dependent dilatation aspect. Hyperhomocysteinemia is an independent cardiovascular risk factor that has been associated with atherosclerotic vascular diseases and ischemic heart attacks. The potential mechanisms by which elevated plasma homocysteine level leads to reduction in nitric oxide bioavailability include the disruptive uncoupling of nitric oxide synthase activity and quenching of nitric oxide by oxidative stress, the enzymatic inhibition by asymmetric dimethylarginine, endoplasmic reticulum stress with eventual endothelial cell apoptosis, and chronic inflammation/prothrombotic conditions. Homocysteine-induced endothelial dysfunction presumably affecting the bioavailability of the potent vasodilator ‘nitric oxide', and such dysfunction can easily be monitor by flow-mediated dilation method using ultrasound. Understanding the mechanisms by which plasma homocysteine alter endothelial nitric oxide production is therefore essential in the comprehension of homocysteine-induced impairment of endothelial dependent dilatation, and its association of cardiovascular risk and its pathophysiology.
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                Author and article information

                Journal
                Journal ID (publisher-id): JVR
                Journal ID (nlm-ta): J Vasc Res
                Journal ID (doi): 10.1159/issn.1018-1172
                Title: Journal of Vascular Research
                Publisher: S. Karger AG
                ISSN (Print): 1018-1172
                ISSN (Electronic): 1423-0135
                Publication date Subscription-year: 2019
                Publication date (Print): October 2019
                Publication date (Electronic): 15 July 2019
                Volume: 56
                Issue: 5
                Pages: 230-240
                Affiliations
                [_a] aDepartment of Vascular and Thyroid Surgery, The First Affiliated Hospital, China Medical University, Shenyang, China
                [_b] bDivision of Vascular Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi, China
                [_c] cDepartment of Cardiothoracic Vascular Surgery, Affiliated Hospital of Beihua University, Jilin City, China
                Author notes
                *Prof. Xinhua Hu, Department of Vascular and Thyroid Surgery, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning 110001 (PR China), E-Mail xinhuahu@126.com
                Article
                Publisher ID: 501313 Other ID: J Vasc Res 2019;56:230–240
                DOI: 10.1159/000501313
                PubMed ID: 31307051
                SO-VID: a7124db2-20b6-4ebc-b0de-125460dec4a5
                Copyright © © 2019 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 04 March 2019
                Date accepted : 04 June 2019
                Page count
                Figures: 4, Tables: 1, Pages: 11
                Categories
                Subject: Research Article

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Abdominal aortic aneurysm,Autophagy,Homocysteine,Matrix metalloproteinase-2,Methionine
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Abdominal aortic aneurysm, Autophagy, Homocysteine, Matrix metalloproteinase-2, Methionine

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