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dc.contributor.authorMoretti, Ana I. S.
dc.contributor.authorSouza Pinto, Francisco J. P.
dc.contributor.authorCury, Vivian
dc.contributor.authorJurado, Marcia C.
dc.contributor.authorMarcondes, Wagner [UNIFESP]
dc.contributor.authorVelasco, Irineu T.
dc.contributor.authorSouza, Heraldo P.
dc.date.accessioned2016-01-24T14:17:42Z
dc.date.available2016-01-24T14:17:42Z
dc.date.issued2012-01-01
dc.identifierhttp://dx.doi.org/10.1016/j.actbio.2011.08.004
dc.identifier.citationActa Biomaterialia. Oxford: Elsevier B.V., v. 8, n. 1, p. 108-115, 2012.
dc.identifier.issn1742-7061
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34443
dc.description.abstractProsthetic meshes are commonly used to correct abdominal wall defects. However, the inflammatory reaction induced by these devices in the peritoneum is not completely understood. We hypothesized that nitric oxide (NO), produced by nitric oxide synthase 2 (NOS2) may modulate the response induced by mesh implants in the abdominal wall and, consequently, affect the outcome of the surgical procedure. Polypropylene meshes were implanted in the peritoneal side of the abdominal wall in wild-type and NOS2-deficient (NOS2(-/-)) mice. After 15 days tissues around the mesh implant were collected, and inflammatory markers (the cytokine interleukin 1 beta (IL-1 beta) and NO) and tissue remodeling (collagen and metalloproteinases (MMP) 2 and 9) were analyzed. the lack of NOS2-derived NO induced a higher incidence of visceral adhesions at the mesh implantation site compared with wild-type mice that underwent the same procedure (P < 0.05). Additionally, higher levels of IL-1 beta were present in the mesh-implanted NOS2(-/-) animals compared with control and wild-type mice. Mesh implantation induced collagen I and III deposition, but in smaller amounts in NOS2(-/-) mice. MMP-9 activity after the surgical procedure was similarly increased in both groups. Conversely, MMP-2 activity was unchanged in mesh-implanted wild-type mice, but was significantly increased in NOS2(-/-) mice (P < 0.01), due to decreased S-nitrosylation of the enzyme in these animals. We conclude that NOS2-derived NO is crucial for an adequate response to and integration of polypropylene mesh implants in the peritoneum. NO deficiency results in a prolonged inflammatory reaction to the mesh implant, and reduced collagen deposition may contribute to an increased incidence of visceral adhesions. (C) 2011 Acta Materialia Inc. Published by Elsevier B.V. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipDIREX LIM
dc.format.extent108-115
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofActa Biomaterialia
dc.rightsAcesso restrito
dc.subjectPolypropylene meshen
dc.subjectInducible nitric oxide synthaseen
dc.subjectNitric oxideen
dc.subjectInflammationen
dc.subjectMatrix metalloproteinasesen
dc.titleNitric oxide modulates metalloproteinase-2, collagen deposition and adhesion rate after polypropylene mesh implantation in the intra-abdominal wallen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Fac Med, Emergency Med Div, São Paulo, Brazil
dc.description.affiliationEscola Paulista Med, Dept Surg, Div Gastrointestinal Surg, UNIFESP, BR-04023 São Paulo, Brazil
dc.description.affiliationUnifespEscola Paulista Med, Dept Surg, Div Gastrointestinal Surg, UNIFESP, BR-04023 São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 2009/01145-1
dc.identifier.doi10.1016/j.actbio.2011.08.004
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000298763500012


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