ABSTRACT
Objective To investigate the relationship between nuclear factor kappa B(NF-κB) and matrix metalloproteinase-9 (MMP-9) mRNA in human umbilical vein endothelial cells(HUVECs) stimulated by the serum from children with coronary artery lesions of Kawasaki disease (KD).Methods HUVECs were cultured and were divided into 4 groups:normal serum group,general fever group,Non-CALs group and CALs group.Co-Immunoprecipitation (ChIP) was used to detect the relationship between NF-κB and MMP-9,and RT-PCR was used to detect the mRNA level of MMP-9.Results Compared with control groups,NF-κB p65 could bind the promoter of MMP 9 in HUVECs cultured with 10 ％ serum from KD patients with coronary artery lesions.The mRNA level of MMP 9 was also up-regulated.Conclusion NF-κB p65 can promote the transcription of MMP-9 in HUVECs induced by the serum from KD patients with coronary artery lesions.
ABSTRACT
Evidence suggests that metalloprotease expression may affect the biological behavior of odontogenic lesions. This study was conducted to review the literature about the role of metalloproteases in the development of odontogenic lesions. A search was carried out using one database, MEDLINE, via PubMed. Only articles written in English were included. Abstracts of all articles retrieved in the electronic search were evaluated for their relevance. Three articles met inclusion criteria. They analyzed the role of MMP-2, MMP-8 and MMP-13 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors, and of MMP-1, MMP-7 and MMP-27 in keratocystic odontogenic tumors. The immunostaining technique used for all studies was similar, differing only in type of staining used. Different immunoreactivity results were found in the studies. The pattern of metalloprotease expression in odontogenic lesions was different from the pattern found in other lesions. In the studies analyzed, there was a significant positive immunoreactivity for metalloproteases in odontogenic lesions, particularly in keratocystic odontogenic tumors, a finding that may explain KCOT aggressiveness.
Evidências sugerem que a expressão das metaloproteinases podem afetar o comportamento biológico das lesões odontogênicas. Esse estudo foi conduzido a fim de revisar a literatura sobre o papel das metaloproteinases no desenvolvimento das lesões odontogênicas. A pesquisa foi realizada utilizando a base de dados do MEDLINE, via PUBMED. Somente artigos escritos em língua inglesa foram aceitos. Os resumos de todos os artigos encontrados na busca foram avaliados de acordo com sua relevância. Três artigos preencheram os critérios de inclusão. Eles analisaram o papel da MMP-2, MMP-8 e MMP-13 nos cistos radiculares, cistos dentígeros e nos tumores odontogênicos ceratocísticos (TOC) e MMP-1, MMP-7 e MMP-27 no TOC. A técnica imunoistoquímica utilizada por todos os estudos foi similar, diferindo somente pelo tipo da coloração utilizada. Diferentes imunomarcações foram encontradas nos estudos. O padrão da expressão das metaloproteinases nas lesões odontogênicos variou entre as lesões. Nos estudos analisados, houve uma imunomarcação positiva, significante estatiticamente, das metaloproteinases nas lesões odontogênicas em especial nos TOCs, o que pode explicar a agressividade dessas lesões.
Subject(s)
Odontogenic Cysts , Immunohistochemistry , Extracellular Matrix , Matrix Metalloproteinases , Odontogenic TumorsABSTRACT
BACKGROUND: Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality amont the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hyopthesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. METHODS: Two groups of five guinea pigs were exposed to the whole smoke of 20 commerical cigarettes per day, 5 hours/day, 5 days/week, for 6 weeks, and 12 weeks, respectively, using a smoking apparatus. Five agematched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically examined(×400) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at 4℃). Two sets of culture plates were loaded with 1×106 intraalveolar cells. One plate, contained 0.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at 37℃. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. RESULTS: At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field (400×) was 121.4±7.2, 158.0±20.2, 196.8±32.8, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, r2=0.675). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDTA. However, the gelatinolytic enzymes were not expressed in the control groups. CONCLUSION: CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic preoteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of gunea pigs.