Genomic analysis of C-fos in Airway Wall of COPD Patients at mRNA level via increase of Reactive Oxygen Species after Countering to Sulfur Mustard
Introduction: The airway epithelium as a physiological barrier defend airway against environmental hazards in lung disease such as Chronic Obstructive Pulmonary Disease (COPD). This defense seems to be regulated via alteration of inflammatory genes and Reactive oxygen species (ROS) have an important...
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Published in | Ṭibb-i jānbāz Vol. 3; no. 2; pp. 46 - 52 |
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Main Authors | , , , |
Format | Journal Article |
Language | Persian |
Published |
Afarand Scholarly Publishing Institute
01.03.2011
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Abstract | Introduction: The airway epithelium as a physiological barrier defend airway against environmental hazards in lung disease such as Chronic Obstructive Pulmonary Disease (COPD). This defense seems to be regulated via alteration of inflammatory genes and Reactive oxygen species (ROS) have an important role in expression of inflammatory proteins. ROS promote the upregulation of cytokines and inflammatory proteins via activation of transcription factors such as Activated Protein 1 (AP-1). Sulfur Mustard (SM) is one of the hazardous agents which cause increase of ROS. In this study we will highlight the role of AP-1 in activation of cytokines and inflammatory molecules following the increase of ROS after exposure to SM in airway wall and for this purpose we chose C-fos which is the most common monodimer of AP-1. Materials and Methods: Ten control individuals and twenty SM exposed patients were considered. RT-PCR and Real-time PCR measured the quantity of C-fos mRNA in control and SM exposed specimens. Results: Although this research showed 2.89 fold changes in expression levels of C-fos in SM exposed patients in compare to normal group, our result was not statistically remarkable (P> 0.05). Discussion: Our evidence suggested that the induction of C-fos is may be because of increase of ROS after exposure to SM and having no statistically remarkable result is might refer to depletion of antioxidants. |
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AbstractList | Introduction: The airway epithelium as a physiological barrier defend airway against environmental hazards in lung disease such as Chronic Obstructive Pulmonary Disease (COPD). This defense seems to be regulated via alteration of inflammatory genes and Reactive oxygen species (ROS) have an important role in expression of inflammatory proteins. ROS promote the upregulation of cytokines and inflammatory proteins via activation of transcription factors such as Activated Protein 1 (AP-1). Sulfur Mustard (SM) is one of the hazardous agents which cause increase of ROS. In this study we will highlight the role of AP-1 in activation of cytokines and inflammatory molecules following the increase of ROS after exposure to SM in airway wall and for this purpose we chose C-fos which is the most common monodimer of AP-1. Materials and Methods: Ten control individuals and twenty SM exposed patients were considered. RT-PCR and Real-time PCR measured the quantity of C-fos mRNA in control and SM exposed specimens. Results: Although this research showed 2.89 fold changes in expression levels of C-fos in SM exposed patients in compare to normal group, our result was not statistically remarkable (P> 0.05). Discussion: Our evidence suggested that the induction of C-fos is may be because of increase of ROS after exposure to SM and having no statistically remarkable result is might refer to depletion of antioxidants. |
Author | A.A. Imani Fooladi S. Yazdani M.H. Karimfar M.R. Nourani |
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SubjectTerms | ap-1 bronchial wall c-fos ros sulfur mustard |
Title | Genomic analysis of C-fos in Airway Wall of COPD Patients at mRNA level via increase of Reactive Oxygen Species after Countering to Sulfur Mustard |
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