Nitric oxide modulates metalloproteinase-2, collagen deposition and adhesion rate after polypropylene mesh implantation in the intra-abdominal wall
Carregando...
Citações na Scopus
13
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCI LTD
Autores
PINTO, Francisco J. P. Souza
MARCONDES, Wagner
Citação
ACTA BIOMATERIALIA, v.8, n.1, p.108-115, 2012
Resumo
Prosthetic 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.
Palavras-chave
Polypropylene mesh, Inducible nitric oxide synthase, Nitric oxide, Inflammation
Referências
- Anderson JM, 2008, SEMIN IMMUNOL, V20, P86, DOI 10.1016/j.smim.2007.11.004
- Arbos MA, 2006, BIOMATERIALS, V27, P758, DOI 10.1016/j.biomaterials.2005.06.027
- Bosca L, 2005, TOXICOLOGY, V208, P249, DOI 10.1016/j.tox.2004.11.035
- Chen Yi, 2008, Tokai J Exp Clin Med, V33, P28
- Crowe MJ, 2000, J INVEST DERMATOL, V115, P3, DOI 10.1046/j.1523-1747.2000.00010.x
- Dash PR, 2007, EXP CELL RES, V313, P3421, DOI 10.1016/j.yexcr.2007.05.030
- Di Vita G, 2006, AM J SURG, V191, P785, DOI 10.1016/j.amjsurg.2005.11.008
- Eu JP, 2000, BIOCHEMISTRY-US, V39, P1040, DOI 10.1021/bi992046e
- Filippin LI, 2009, NITRIC OXIDE-BIOL CH, V21, P157, DOI 10.1016/j.niox.2009.08.002
- Forbes SS, 2009, BRIT J SURG, V96, P851, DOI 10.1002/bjs.6668
- Frick Chris, 2006, J Long Term Eff Med Implants, V16, P423
- Godoy LC, 2010, SHOCK, V33, P626, DOI 10.1097/SHK.0b013e3181cb88e6
- Goldenberg Alberto, 2005, Acta Cir Bras, V20, P347
- Gu ZZ, 2002, SCIENCE, V297, P1186, DOI 10.1126/science.1073634
- Hinkle CL, 2003, BIOCHEMISTRY-US, V42, P2127, DOI 10.1021/bi026709v
- Hsu YC, 2007, NITRIC OXIDE-BIOL CH, V16, P258, DOI 10.1016/j.niox.2006.09.002
- Hsu YC, 2006, NITRIC OXIDE-BIOL CH, V14, P327, DOI 10.1016/j.niox.2006.01.006
- Jansen PL, 2007, FASEB J, V21, P1047, DOI 10.1096/fj.06-6755com
- Jones JA, 2007, J BIOMED MATER RES A, V83A, P585, DOI 10.1002/jbm.a.31221
- Jones JA, 2008, J BIOMED MATER RES A, V84A, P158, DOI 10.1002/jbm.a.31220
- Junge K, 2009, J INVEST SURG, V22, P256, DOI 10.1080/08941930802713092
- Kondo Y, 2008, INVEST OPHTH VIS SCI, V49, P4850, DOI 10.1167/iovs.08-1897
- Kyriakides TR, 2009, MATRIX BIOL, V28, P65, DOI 10.1016/j.matbio.2009.01.001
- Li W, 2004, MOL BIOL CELL, V15, P294
- LIEW FY, 1995, ADV NEUROIMMUNOL, V5, P201, DOI 10.1016/0960-5428(95)00009-Q
- Luttikhuizen DT, 2006, BIOMATERIALS, V27, P5763, DOI 10.1016/j.biomaterials.2006.07.004
- Mannick JB, 1999, SCIENCE, V284, P651, DOI 10.1126/science.284.5414.651
- Moilanen E, 1997, AM J PATHOL, V150, P881
- Moretti AIS, 2007, FREE RADIC BIOL MED, V43, P142
- Moretti AIS, 2008, FREE RADIC BIOL MED, V45, P135
- Moretti AIS, 2009, PANCREAS, V38, P507, DOI 10.1097/MPA.0b013e31819fef75
- Okamoto T, 2004, BIOL CHEM, V385, P997, DOI 10.1515/BC.2004.130
- Page-McCaw A, 2007, NAT REV MOL CELL BIO, V8, P221, DOI 10.1038/nrm2125
- Patel JD, 2007, J BIOMED MATER RES A, V80A, P381, DOI 10.1002/jbm.a.30907
- Rajagopalan S, 1996, J CLIN INVEST, V98, P2572, DOI 10.1172/JCI119076
- Reiss MJ, 2009, WOUND REPAIR REGEN, V17, P418, DOI 10.1111/j.1524-475X.2009.00476.x
- Saed GM, 2004, J AM ASSOC GYN LAP, V11, P307, DOI 10.1016/S1074-3804(05)60041-2
- Saed GM, 2006, HUM REPROD, V21, P1605, DOI 10.1093/humrep/dei500
- Schulz DD, 2009, ACTA CIR BRAS, V24, P476
- Shapiro SD, 1999, AM J RESP CELL MOL, V20, P1100
- Shukla A, 1999, MOL CELL BIOCHEM, V200, P27, DOI 10.1023/A:1006977513146
- Sitia G, 2004, J CLIN INVEST, V113, P1158, DOI 10.1172/JCI200421087
- Vaz Marcia, 2009, Acta Cir Bras, V24, P19
- Visse R, 2003, CIRC RES, V92, P827, DOI 10.1161/01.RES.0000070112.80711.3D
- Wani J, 2007, BIOL CHEM, V388, P497, DOI 10.1515/BC.2007.056
- Weyhe D, 2007, WORLD J SURG, V31, P234, DOI 10.1007/s00268-006-0123-4
- Yamasaki K, 1998, J CLIN INVEST, V101, P967, DOI 10.1172/JCI2067