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The role of MMP-9 and TIMP-1 in nasal polyp formation. Swiss medical weekly : official journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology [Swiss Med Wkly] Journal article

 
TitleThe role of MMP-9 and TIMP-1 in nasal polyp formation.
Author(s)Kahveci O, Derekoy F, Yilmaz M, Serteser M, Altuntas A 
InstitutionAfyon Kocatepe University, Faculty of Medicine, Department of Otolaryngology, Afyon, Turkey. orhangs75@hotmail.com.
SourceSwiss Med Wkly 2008 Nov 15; 138(45-46):684-8.
AbstractOBJECTIVE: The complex structure of polyp formation is still unknown. Matrix metalloproteinases (MMPs), a family of zinc-dependant endopeptidases with proteolytic activities towards several components of extracellular matrix, play an important role in connective tissue remodeling. Tissue inhibitors of matrix metalloproteinases (TIMPs) are natural inhibitors of MMPs. The balance between MMP/TIMP is very critical in matrix remodeling and various physiological processes. Imbalances between these enzymes and inhibitors may cause pathological processes such as chronic inflammation, degenerative disease and tumour invasion. In our study we aimed at demonstrating MMP/TIMP imbalance in nasal polyposis, similar to other pathological processes. STZUDY
DESIGN AND SETTING: Nasal polyp specimens were obtained from twenty patients with nasal polyposis during endoscopic sinus surgery. Bullous middle turbinates with normal appearing mucosa of fifteen non-smoker patients free of any allergic or infectious diseases of nose or sinuses were used as controls. We measured the MMP-9 and TIMP-1 levels in tissue specimens using an ELISA method.
RESULTS: MMP-9 levels were significantly increased and TIMP-1 levels were significantly decreased in polyp tissues in comparison to controls with no correlation observed between MMP-9 levels and inflammatory cell populations.
CONCLUSION: MMP-9 and TIMP-1 may play an active pathogenic role in nasal polyp formation. MMP-9 levels are regulated independently from inflammatory cell populations.
Languageeng
Pub Type(s)Journal Article
PubMed ID19043814
  
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