Significance of serum matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in chronic hepatitis C patients

Badra, Gamal; Lotfy, Mahmoud; El-Refaie, A.; Obada, Moanis; Abdelmonem, Elhamy; Kandeel, Samia H; Fathy, Amr A

doi:10.1556/amicr.57.2010.1.3

Cited by 33 publications

(24 citation statements)

References 26 publications

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“…Diverse intensity and progression of airway inflammation between studied COPD groups could be responsible for these discrepancies. As has been shown in patients with liver diseases, those with chronic hepatitis C exhibited high serum MMP-9 concentrations, which decreased to the nadir in subjects with liver cirrhosis, while TIMP-1 concentrations significantly increased, serving as a marker of fibrotic changes [25]. This suggests that the proteases/antiproteases balance may depend on and change with the progression of disease.…”

Section: Discussionmentioning

confidence: 80%

Enhanced Exhalation of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 in Patients with COPD Exacerbation: A Prospective Study

Kwiatkowska¹,

Noweta²,

Zieba

et al. 2012

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Background: Matrix metalloproteinase-9 (MMP-9) and its inhibitor tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the pathogenesis of airway inflammation in patients with chronic obstructive pulmonary disease (COPD). However, no study so far has addressed their value as noninvasive biomarkers of airways inflammation. Objective: To evaluate MMP-9 and TIMP-1 concentrations in the exhaled breath condensate (EBC) of patients with stable COPD and also during the exacerbation episode. Methods: EBC and serum samples were collected in 17 stable-phase COPD patients who were current smokers as well as during their first exacerbation episode, and in 22 asymptomatic smokers. EBC and serum levels of MMP-9 and TIMP-1 were measured with ELISA kit. Results: Mean EBC MMP-9 and TIMP-1 levels were higher in patients with stable COPD than in asymptomatic smokers. Exacerbation of COPD increased 2-fold the exhalation of MMP-9 (18.5 ± 10.1 ng/ml vs. 8.9 ± 6.2 ng/ml, p = 0.01) and TIMP-1 (to 41.1 ± 20.4 ng/ml vs. 16.4 ± 6.8 ng/ml, p < 0.001). Both, MMP-9 and TIMP-1 in EBC correlated negatively with FEV₁ (% predicted) at baseline (r = –0.78, p < 0.001 and r = –0.73, p < 0.001) and during the exacerbation episode (r = –0.57, p = 0.02 and r = –0.65, p = 0.005). Similar negative correlations were noted with FVC (% predicted), except for MMP-9 in EBC at exacerbation. Exhaled MMP-9 and TIMP-1 did not correlate with serum concentrations in COPD patients, either at baseline or during exacerbation. Conclusion: Exhaled MMP-9 and TIMP-1 increased during COPD exacerbation and was negatively correlated with spirometric variables, which suggests the usefulness of their measurement in EBC for the monitoring of airways inflammation. However, to better assess their diagnostic or prognostic value larger studies are necessary.

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Section: Discussionmentioning

confidence: 80%

Enhanced Exhalation of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 in Patients with COPD Exacerbation: A Prospective Study

Kwiatkowska¹,

Noweta²,

Zieba

et al. 2012

Respiration

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“…In contrast to MMP-2, MMP-9 levels show their value primarily in the diagnosis of hepatocellular carcinoma [62]. In one of the studies, MMP-9 levels were negatively correlated to the histological severity of the liver disease in patients with chronic hepatitis C [63]. …”

Section: Diagnostics Of Acquired Liver Fibrosismentioning

confidence: 99%

“…For example, chronic hepatitis C causes the elevation of both TIMP-1 and TIMP-2 in corollary with fibrosis progression [60]. A recent study of the relationship between serum MMP-9, TIMP-1 and fibrosis in 50 patients with various chronic liver disease showed that serum levels of MMP-9 in chronic hepatitis patients were low as compared to the controls ( P < 0.05) [63]. Moreover, serum MMP-9 levels decrease as chronic hepatitis progresses to cirrhosis, while TIMP-1 levels increase along with an increase of the degree of fibrosis (r = 0.73, P < 0.001).…”

Section: Diagnostics Of Acquired Liver Fibrosismentioning

confidence: 99%

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Non-Invasive markers for hepatic fibrosis

et al. 2011

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With great advancements in the therapeutic modalities used for the treatment of chronic liver diseases, the accurate assessment of liver fibrosis is a vital need for successful individualized management of disease activity in patients. The lack of accurate, reproducible and easily applied methods for fibrosis assessment has been the major limitation in both the clinical management and for research in liver diseases. However, the problem of the development of biomarkers capable of non-invasive staging of fibrosis in the liver is difficult due to the fact that the process of fibrogenesis is a component of the normal healing response to injury, invasion by pathogens, and many other etiologic factors. Current non-invasive methods range from serum biomarker assays to advanced imaging techniques such as transient elastography and magnetic resonance imaging (MRI). Among non-invasive methods that gain strongest clinical foothold are FibroScan elastometry and serum-based APRI and FibroTest. There are many other tests that are not yet widely validated, but are none the less, promising. The rate of adoption of non-invasive diagnostic tests for liver fibrosis differs from country to country, but remains limited. At the present time, use of non-invasive procedures could be recommended as pre-screening that may allow physicians to narrow down the patients' population before definitive testing of liver fibrosis by biopsy of the liver. This review provides a systematic overview of these techniques, as well as both direct and indirect biomarkers based approaches used to stage fibrosis and covers recent developments in this rapidly advancing area.

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“…Some genes were found to play critical roles in these processes, including MMP9, TIMP1 and STAT1 [8-11]. However, the spectrum of temporal pathway deregulation has rarely been studied using a systematic framework.…”

Section: Introductionmentioning

confidence: 99%

Integrative network analysis identifies key genes and pathways in the progression of hepatitis C virus induced hepatocellular carcinoma

et al. 2011

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BackgroundIncidence of hepatitis C virus (HCV) induced hepatocellular carcinoma (HCC) has been increasing in the United States and Europe during recent years. Although HCV-associated HCC shares many pathological characteristics with other types of HCC, its molecular mechanisms of progression remain elusive.MethodsTo investigate the underlying pathology, we developed a systematic approach to identify deregulated biological networks in HCC by integrating gene expression profiles with high-throughput protein-protein interaction data. We examined five stages including normal (control) liver, cirrhotic liver, dysplasia, early HCC and advanced HCC.ResultsAmong the five consecutive pathological stages, we identified four networks including precancerous networks (Normal-Cirrhosis and Cirrhosis-Dysplasia) and cancerous networks (Dysplasia-Early HCC, Early-Advanced HCC). We found little overlap between precancerous and cancerous networks, opposite to a substantial overlap within precancerous or cancerous networks. We further found that the hub proteins interacted with HCV proteins, suggesting direct interventions of these networks by the virus. The functional annotation of each network demonstrates a high degree of consistency with current knowledge in HCC. By assembling these functions into a module map, we could depict the stepwise biological functions that are deregulated in HCV-induced hepatocarcinogenesis. Additionally, these networks enable us to identify important genes and pathways by developmental stage, such as LCK signalling pathways in cirrhosis, MMP genes and TIMP genes in dysplastic liver, and CDC2-mediated cell cycle signalling in early and advanced HCC. CDC2 (alternative symbol CDK1), a cell cycle regulatory gene, is particularly interesting due to its topological position in temporally deregulated networks.ConclusionsOur study uncovers a temporal spectrum of functional deregulation and prioritizes key genes and pathways in the progression of HCV induced HCC. These findings present a wealth of information for further investigation.

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Significance of serum matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in chronic hepatitis C patients

Cited by 33 publications

References 26 publications

Enhanced Exhalation of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 in Patients with COPD Exacerbation: A Prospective Study

Enhanced Exhalation of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 in Patients with COPD Exacerbation: A Prospective Study

Non-Invasive markers for hepatic fibrosis

Integrative network analysis identifies key genes and pathways in the progression of hepatitis C virus induced hepatocellular carcinoma

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