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Fluorescent Analysis of Asthma Associated Mucin Protein Expression Exposure to Environmental Contaminants

Status Complete
Seeking Researchers No
Start Date 09/01/2005
End Date 06/30/2006
Funding Source Undergraduate Research Grants
Funding Amount
Community Partner
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Last Updated 07/05/2008 01:25AM
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Faculty
  Carol Jones

Student Researchers
  Reem Sheikh

Abstract

Asthma is a chronic respiratory illness caused by inflammation of lung tissue and its episodes have dramatically increased within the past two decades. Asthmatic patients exhibit mucus over-production, which can cause overall decreased lung function and development of severe symptoms, Mucus in lung epithelia is produced by mucin glycoproteins that are primarily produced by the MUC1, MUC5AC, and MUC5B genes. Research has shown an increase in lung inflammation and asthma in people exposed to environmental carcinogens, particularly those found in cigarette smoke and car exhaust. These contaminants both contain polycyclic aromatic hydrocarbons (PAH) that stimulate the aryl hydrocarbon receptor (AhR) response. Also, a highly toxic PAH, 2, 3, 7, 8-tetrachlor-odibenzo-p-dioxin (TCDD) has shown to activate the AhR and induce immune response. Last Spring, I investigated the molecular pathway between TCDD- activated AhR and mucin genes found in lung epithelia (MUC1, MUC5B, MUC5AC). To continue investigating a molecular pathway connecting asthma to environmental carcinogens, production and location of mucin proteins from MUC1, MUC5B and MUC5AC expression after TCDD exposure to A459 cells will be analyzed through immunofluorescence microscopy. DNA expression of mucin genes was analyzed during Spring 2005 and now protein production and location within the cell will be studied. Changes in mucin protein location may suggest how asthmatic patients react to allergy attacks based on TCDD exposure time and concentration. We hypothesize that production and localization of mucin core proteins in A459 cells will vary in relation to TCDD-dose and time dependent treatments.

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