Inducible nitric oxide synthase inhibition increases MMP-2 activity leading to imbalance between extracellular matrix deposition and degradation after polypropylene mesh implant

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorSOUZA-PINTO, Franciso J. P.
dc.contributor.authorMORETTI, Ana I. S.
dc.contributor.authorCURY, Vivian
dc.contributor.authorMARCONDES, Wagner
dc.contributor.authorVELASCO, Irineu T.
dc.contributor.authorSOUZA, Heraldo P.
dc.date.accessioned2013-09-23T16:36:01Z
dc.date.available2013-09-23T16:36:01Z
dc.date.issued2013
dc.description.abstractProsthetic mesh implants are commonly used to correct abdominal wall defects. However, success of the procedure is conditioned by an adequate inflammatory response to the device. We hypothesized that nitric oxide produced by nitric oxide synthase 2 (NOS2) and MMP-2 and -9 participate in response induced by mesh implants in the abdominal wall and, consequently, affect the outcome of the surgical procedure. In the first step, temporal inflammatory markers profile was evaluated. Polypropylene meshes were implanted in the peritoneal side of the abdominal wall of C57Black mice. After 2, 4, 7, 15, and 30 days, tissues around the mesh implant were collected and inflammatory markers were analyzed. In the second step, NOS2 activity was inhibited with nitro-L-arginine methyl ester (L-NAME). Samples were collected after 15 days (when inflammation was reduced), and the inflammatory and tissue remodeling markers were investigated. Polypropylene mesh implant induced a pro-inflammatory environment mediated by intense MMP-2 and -9 activities, NO release, and interleukin-1 production peaking in 7 days and gradually decreasing after 15 days. NOS2 inhibition increased MMP-2 activity and resulted in a higher visceral adhesion incidence at the mesh implantation site when compared with non-treated animals that underwent the same procedure. We conclude that NOS2-derived NO is crucial for adequate response to polypropylene mesh implant integration in the peritoneum. NO deficiency results in an imbalance between extracellular matrix deposition/degradation contributing to visceral adhesions incidence. (c) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2013.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo-FAPESP
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico-CAPES
dc.description.sponsorshipDIREX LIM [FMUSP-HC/LIMs]
dc.identifier.citationJOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A, v.101A, n.5, p.1379-1387, 2013
dc.identifier.doi10.1002/jbm.a.34440
dc.identifier.issn1549-3296
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/1728
dc.language.isoeng
dc.publisherWILEY-BLACKWELL
dc.relation.ispartofJournal of Biomedical Materials Research Part A
dc.rightsrestrictedAccess
dc.rights.holderCopyright WILEY-BLACKWELL
dc.subjectpolypropylene mesh
dc.subjectinflammation
dc.subjectinducible nitric oxide synthase
dc.subjectnitric oxide
dc.subjectmatrix metalloproteinases
dc.subject.otherforeign-body reaction
dc.subject.others-nitrosylation
dc.subject.otherhernia repair
dc.subject.othermetalloproteinases
dc.subject.othercollagen
dc.subject.othercells
dc.subject.othermodel
dc.subject.otherbiomaterials
dc.subject.othermacrophages
dc.subject.othersepsis
dc.subject.wosEngineering, Biomedical
dc.subject.wosMaterials Science, Biomaterials
dc.titleInducible nitric oxide synthase inhibition increases MMP-2 activity leading to imbalance between extracellular matrix deposition and degradation after polypropylene mesh implant
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalSOUZA-PINTO, Franciso J. P.:Univ Sao Paulo, Fac Med, Div Emergency Med, BR-01246903 Sao Paulo, Brazil
hcfmusp.author.externalMARCONDES, Wagner:Univ Fed Sao Paulo, Dept Surg, Div Gastrointestinal Surg, Escola Paulista Med, Sao Paulo, Brazil
hcfmusp.citation.scopus8
hcfmusp.contributor.author-fmusphcANA IOCHABEL SOARES MORETTI
hcfmusp.contributor.author-fmusphcVIVIAN CURY
hcfmusp.contributor.author-fmusphcIRINEU TADEU VELASCO
hcfmusp.contributor.author-fmusphcHERALDO POSSOLO DE SOUZA
hcfmusp.description.beginpage1379
hcfmusp.description.endpage1387
hcfmusp.description.issue5
hcfmusp.description.volume101A
hcfmusp.origemWOS
hcfmusp.origem.pubmed23077110
hcfmusp.origem.scopus2-s2.0-84884212774
hcfmusp.origem.wosWOS:000316815700018
hcfmusp.publisher.cityHOBOKEN
hcfmusp.publisher.countryUSA
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hcfmusp.remissive.sponsorshipCAPES
hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFMUSP-HC
hcfmusp.scopus.lastupdate2024-05-17
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