Project description:A total of 30 days of exposure to cigarette smoke (CS) or indoor air was given to 8- 23 week-old female C57BL/6 mice, then proteomics analyses were used to determine the 24 impact of CS on ovarian reserve.
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.
Project description:Cigarette smoke exposure induces pulmonary inflammation despite increased risk of lung infection. We tested the ability of human beta-defensin 2, an antimicrobial peptide, to modulate inflammatory processes while promoting immune competence.
Project description:The goal of this project is to identify novel genes that contribute to inflammation in cigarette smoke induced chronic obstructive pulmonary disease (COPD). Our lab is interested in a class of RNA genes called Long noncoding RNAs (lncRNAs). There are over 16,000 lncRNAs in the human genome and less than 3% have defined functions. Here we aim to identify inflammatory specific lncRNAs that are dysregulated following cigarette smoke exposure in macrophages.
Project description:Endothelial cells (HUVEC) were exposed to cigarette smoke extract for 3, 7, and 24 hours. Total RNA was isolated and used for hybridisation to dual channel oligonucleotide genome-wide microarrays using untreated HUVEC as a control. The objective was to find out what genes are regulated by exposure to cigarette smoke extract, and the time dependency of their regulation Keywords: time course, stress response
Project description:Smoking is the leading cause of preventable death worldwide. It increases the risk for various diseases including respiratory diseases, vascular diseases and different cancers including lung, oral and bladder cancer. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon cigarette smoke exposure are yet to be fully elucidated. It is crucial to note that disease development is observed upon chronic exposure to cigarette smoke, as opposed to a short-term exposure. Hence, we sought to investigate the effect of chronic smoke exposure on normal oral keratinocytes (OKF6/TERT1). We employed tandem mass tag-based quantitative proteomic and phosphoproteomic approaches to investigate the proteomic and signaling changes in OKF6/TERT1 cells chronically exposed to cigarette smoke compared to untreated cells. LC/MS2 analysis resulted in the quantification of 5,067 proteins among which expression of 360 proteins were found to be dysregulated in at least one replicate. Phosphoproteomic analysis revealed quantification of 3,647 phosphopeptides corresponding to 1,801 proteins. Majority of the dysregulated proteins were seen to be involved in cellular processes such as cell growth, cellular communication and energy metabolism. This study will aid in elucidating the effects of smoking in oral cancer and in the identification of potential candidates molecules which could serve as early detection biomarkers or therapeutic targets.
Project description:Mycbacterium tuberculosis was exposed to cigarette smoke condensate (CSC) in 7H9 dextrose culture media. The transcriptional response to cigarette smoke condensate was compared to that of exposure to the CSC diluent, DMSO..