Publication:
Vasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses.

dc.contributor.authorBenitez, Raquel
dc.contributor.authorDelgado-Maroto, Virginia
dc.contributor.authorCaro, Marta
dc.contributor.authorForte-Lago, Irene
dc.contributor.authorDuran-Prado, Mario
dc.contributor.authorO'Valle, Francisco
dc.contributor.authorLichtman, Andrew H
dc.contributor.authorGonzalez-Rey, Elena
dc.contributor.authorDelgado, Mario
dc.date.accessioned2023-01-25T10:06:59Z
dc.date.available2023-01-25T10:06:59Z
dc.date.issued2018-04-18
dc.description.abstractVasoactive intestinal peptide (VIP) is a neuropeptide that exerts various vascular and cardioprotective functions and regulates immune function and inflammatory response at multiple levels. However, its role in inflammatory cardiovascular disorders is largely unknown. Myocarditis and atherosclerosis are two inflammatory and autoimmune cardiovascular diseases that cause important adverse circulatory events. In this study, we investigate the therapeutic effects of VIP in various well-established preclinical models of experimental autoimmune myocarditis and atherosclerosis. Intraperitoneal injection of VIP during the effector phase of experimental autoimmune myocarditis in susceptible BALB/c mice significantly reduced its prevalence, ameliorated signs of heart hypertrophy and injury, attenuated myocardial inflammatory infiltration, and avoided subsequent profibrotic cardiac remodeling. This effect was accompanied by a reduction of Th17-driven cardiomyogenic responses in peripheral lymphoid organs and in the levels of myocardial autoantibodies. In contrast, acute and chronic atherosclerosis was induced in apolipoprotein E-deficient mice fed a hyperlipidemic diet and subjected to partial carotid ligation. Systemic VIP treatment reduced the number and size of atherosclerotic plaques in carotid, aorta, and sinus in hypercholesterolemic mice. VIP reduced Th1-driven inflammatory responses and increased regulatory T cells in atherosclerotic arteries and their draining lymph nodes. VIP also regulated cholesterol efflux in macrophages and reduced the formation of foam cells and their presence in atherosclerotic plaques. Finally, VIP inhibited proliferation and migration of smooth muscle cells and neointima formation in a mouse model of complete carotid ligation. These findings encourage further studies aimed to assess whether VIP can be used as a pharmaceutical agent to treat heart inflammation and atherosclerosis.
dc.identifier.doi10.4049/jimmunol.1800122
dc.identifier.essn1550-6606
dc.identifier.pmid29669783
dc.identifier.unpaywallURLhttps://www.jimmunol.org/content/jimmunol/200/11/3697.full.pdf
dc.identifier.urihttp://hdl.handle.net/10668/12366
dc.issue.number11
dc.journal.titleJournal of immunology (Baltimore, Md. : 1950)
dc.journal.titleabbreviationJ Immunol
dc.language.isoen
dc.organizationIBS
dc.page.number3697-3710
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, Non-U.S. Gov't
dc.rights.accessRightsopen access
dc.subject.meshAnimals
dc.subject.meshApolipoproteins E
dc.subject.meshAtherosclerosis
dc.subject.meshAutoantibodies
dc.subject.meshAutoimmune Diseases
dc.subject.meshAutoimmunity
dc.subject.meshDisease Models, Animal
dc.subject.meshFemale
dc.subject.meshInflammation
dc.subject.meshLymph Nodes
dc.subject.meshMacrophages
dc.subject.meshMale
dc.subject.meshMice
dc.subject.meshMice, Inbred BALB C
dc.subject.meshMice, Inbred C57BL
dc.subject.meshMuscle, Smooth
dc.subject.meshMyocarditis
dc.subject.meshMyocardium
dc.subject.meshNeuropeptides
dc.subject.meshT-Lymphocytes, Regulatory
dc.subject.meshTh17 Cells
dc.subject.meshVasoactive Intestinal Peptide
dc.titleVasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number200
dspace.entity.typePublication

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