ArticleRespiratory research2009
MMP/TIMP expression profiles in distinct lung disease models: implications for possible future therapies.
Article in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
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- Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors.Respiratory research · 2017Article
- The role of adenylyl cyclase isoform 6 in β-adrenoceptor signalling in murine airways.British journal of pharmacology · 2015Article
- TLR4 activation induces IL-1β release via an IPAF dependent but caspase 1/11/8 independent pathway in the lung.Respiratory research · 2014Article
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- Requirement for inducible nitric oxide synthase in chronic allergen exposure-induced pulmonary fibrosis but not inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Differential effects of dexamethasone and rosiglitazone in a sephadex-induced model of lung inflammation in rats: possible role of tissue inhibitor of metalloproteinase-3.Indian journal of pharmacologyArticle
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThere is currently a vast amount of evidence in the literature suggesting that matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are involved in the pathogenesis of inflammatory airways diseases, such as asthma and COPD. Despite this, the majority of reports only focus on single MMPs, often only in one model system. This study aimed to investigate the profile of an extensive range of MMP/TIMP levels in three different pre-clinical models of airways disease. These models each have a different and very distinct inflammatory profile, each exhibiting inflammatory characteristics that are similar to that observed in asthma or COPD. Since these models have their own characteristic pathophysiological phenotype, one would speculate that the MMP/TIMP expression profile would also be different.
methodsWith the use of designed and purchased MMP/TIMP assays, investigation of rat MMP-2, 3, 714 and TIMP-14 mRNA expression was undertaken by Real Time PCR. The three rodent models of airways disease investigated were the endotoxin model, elastase model, and the antigen model.
resultsIntriguingly, we demonstrated that despite the distinct inflammatory profile observed by each model, the MMP/TIMP expression profile is similar between the models, in that the same MMPs/TIMPs were observed to be generally increased or decreased in all three models. It could therefore be speculated that in a particular disease, it may be a complex network of MMPs, rather than an individual MMP, together with inflammatory cytokines and other mediators, that results in the distinct phenotype of inflammatory diseases, such as asthma and COPD.
conclusionWe believe our data may provide key information necessary to understand the role of various MMPs/TIMPs in different inflammatory airway diseases, and aid the development of more selective therapeutics without the side effect profile of current broad-spectrum MMP inhibitors.
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