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Undergraduate Research Project Management System

Contribution of Activated Aryl Hydrocarbon Receptor to Mucin Gene Expression Associated with Asthma

Status Complete
Seeking Researchers No
Start Date 09/01/2004
End Date 06/30/2005
Funding Source N/A
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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. However, the molecular pathway connecting PAH exposure and asthma is unclear. I hypothesize that induction of AhR signaling by PAH's contributes to asthma by increasing the mucin gene expression in lung epithelia. Dioxin, a potent PAH activator of the AhR, is being used to examine the activation of the MUC 1, MUC5AC, MUC5B genes involving 24 hour treatment of human lung cells (A549 cell line). Differences in cell morphology and gene expression are also being studied in two different media conditions in order to help distinguish AhR-dependent changes in mucin gene expression from those changes induced by serum factors.

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