Presentation Title

Oxidative Stress Induced Histone Glutathionylation and Lung Inflammation of COPD

Presenter Information

Kevin J. SantosFollow

Start Date

November 2016

End Date

November 2016

Location

HUB 302-#178

Type of Presentation

Poster

Abstract

Chronic obstructive pulmonary disease (COPD) is a progressive disease that is characterized by difficulty breathing. This difficulty can be attributed to only small amounts of air being able to get into the lungs. Many abnormalities can cause this lack of air, some of which are loss of elasticity, thickening, and inflammation of the airways. COPD is the third leading cause of death in the United States, with cigarette smoking being the leading cause of it. The leading cause of COPD is cigarette smoking. Previous research has found that cigarette smoke can contain around 1014 free radicals per puff; making cigarettes a large source of free radicals on the lungs. Free radicals are the cause of nitrosative stress. They have been implicated in initiating an inflammatory response in the lung. Glutathione, the cells most important and abundant antioxidant, is a critical component of antioxidant defense mechanism. When oxidized glutathione will form glutathione disulfide. If brought to high enough concentrations in response to the nitrosative/oxidative stress, glutathione disulfide can induce glutathionylation in the nucleus. This study proposes that histone glutathionylation is brought about and influences gene expression. This epigenetic modification can effect the transcription of certain proteins and bring about loss of function of the effected cell. First, we must establish in vitro model. A549 lung cell were treated with DETA-NO (Nitric Oxide is present in cigarette smoke up to concentrations of 1000ppm), at varying concentrations. They were then tested for viability with the use of an MTT assay. Once a LD50 was established, histones from oxidative stress induced cells, at various LDs, will be isolated and probed for glutathionylation through Western blots.

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Oxidative Stress Induced Histone Glutathionylation and Lung Inflammation of COPD

HUB 302-#178

Chronic obstructive pulmonary disease (COPD) is a progressive disease that is characterized by difficulty breathing. This difficulty can be attributed to only small amounts of air being able to get into the lungs. Many abnormalities can cause this lack of air, some of which are loss of elasticity, thickening, and inflammation of the airways. COPD is the third leading cause of death in the United States, with cigarette smoking being the leading cause of it. The leading cause of COPD is cigarette smoking. Previous research has found that cigarette smoke can contain around 1014 free radicals per puff; making cigarettes a large source of free radicals on the lungs. Free radicals are the cause of nitrosative stress. They have been implicated in initiating an inflammatory response in the lung. Glutathione, the cells most important and abundant antioxidant, is a critical component of antioxidant defense mechanism. When oxidized glutathione will form glutathione disulfide. If brought to high enough concentrations in response to the nitrosative/oxidative stress, glutathione disulfide can induce glutathionylation in the nucleus. This study proposes that histone glutathionylation is brought about and influences gene expression. This epigenetic modification can effect the transcription of certain proteins and bring about loss of function of the effected cell. First, we must establish in vitro model. A549 lung cell were treated with DETA-NO (Nitric Oxide is present in cigarette smoke up to concentrations of 1000ppm), at varying concentrations. They were then tested for viability with the use of an MTT assay. Once a LD50 was established, histones from oxidative stress induced cells, at various LDs, will be isolated and probed for glutathionylation through Western blots.