Exposure to cigarette smoke is responsible for a considerable amount of pulmonary diseases including chronic bronchitis, emphysema, carcinoma of the lung, and chronic obstructive pulmonary disease (COPD) and excessive alcohol consumption also contributes to the comorbidities associated with these diseases. COPD is the only chronic disease growing in mortality in the USA and afflicts over 23 million people where at least 12 million remains undiagnosed. Furthermore, veterans are much more likely than non-veterans to have ever smoked (74% compared to 48%). By estimation of the US Department of Veteran Affairs, chronic inflammatory disorder, including asthma and COPD, is a common problem among veterans, accounting for ∼ 16% of VA hospital admissions and a third of admissions to all VA medical services, driving the need to develop novel research strategies to address the pathogenesis of these disorders. Our lab focuses on mechanisms controlling repair of bronchial epithelium particularly, adenosine signal pathway and its role of epithelial injury in airway diseases associated with cigarette smoke and/or in combination with alcohol exposure. Adenosine, an endogenous nucleoside has been recognized as an important modulator of hypoxic, ischemic and inflammatory process critical to both tissue homeostasis and tissue injury. However, the mechanisms by which adenosine-mediated airway wound healing and repair occurs after exposure to injurious agents like cigarette smoke has not been investigated. In addition to understanding the mechanisms involved in adenosine-mediated wound repair our lab has a growing interest in targeting efforts to reduce existing disparities in mortality rates particularly associated with smoke-related lung diseases and lung cancer. We recognized mortality from all causes is higher for persons with fewer years of education and for minorities including but not limited to Black and Hispanic population still remains unknown, which diseases contribute most to these disparities.
We are interested in understanding the dynamics of the receptor-mediated action of adenosine as well as investigating adenosines mechanistic signaling pathways associated with ciliary motility and clearance, pro-and- anti-inflammatory cytokine production, cell adhesion and remodeling and wound repair under conditions of cigarette smoke and/or alcohol exposure, and oxidative stress. In addition, our lab will focus on developing new therapeutic drug target and delivery systems as it relates to airway injury and repair via adenosine signaling pathway. We believe the distribution and varied effects of adenosine receptors in the epithelial airway could have for the most part, important implication in understanding chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD) and smoke-related lung cancer.
Methodology incorporated in our lab includes but not limited to:
• Receptor-Ligand binding Studies
• 3H Thymidine Incorporation Studies
• Molecular Biology Techniques i.e., Western Blots, immunoprecipations assays
• Genetic manipulations (Transfections)
• Ciliary Motility Studies (SAVA)
• Kinase Studies (PKA, PKC and PKG)
• Small animal studies (In vivo and Ex vivo)