PubMed Health⌕ Search

Biomedical subjects

Larry W Tsai

Publications and source records attributed to Larry W Tsai.

3 recordsLinked to original sources

Epithelial cell PPAR[gamma] contributes to normal lung maturation.

Peroxisome proliferator-activated receptor (PPAR)-gamma is a member of the nuclear hormone receptor superfamily that can promote cellular differentiation and organ development. PPARgamma expression has been reported in a number of pulmonary cell types, including inflammatory, mesenchymal, and epithelial cells. We find that PPARgamma is prominently expressed in the airway epithelium in the mouse lung. In an effort to define the physiological role of PPARgamma within the lung, we have ablated PPARgamma using a novel line of mice capable of specifically targeting the airway epithelium. Airway epithelial cell PPARgamma-targeted mice display enlarged airspaces resulting from insufficient postnatal lung maturation. The increase in airspace size is accompanied by alterations in lung physiology, including increased lung volumes and decreased tissue resistance. Genome-wide expression profiling reveals a reduction in structural extracellular matrix (ECM) gene expression in conditionally targeted mice, suggesting a disruption in epithelial-mesenchymal interactions necessary for the establishment of normal lung structure. Expression profiling of airway epithelial cells isolated from conditionally targeted mice indicates PPARgamma regulates genes encoding known PPARgamma targets, additional lipid metabolism enzymes, and markers of cellular differentiation. These data reveal airway epithelial cell PPARgamma is necessary for normal lung structure and function.

Animals↗

Respiratory impedance following bronchoscopic or surgical lung volume reduction for emphysema.

BACKGROUND: Bronchoscopic methods for achieving lung volume reduction (BLVR) are presently undergoing clinical trials, and will soon be clinically available. Understanding the differential effects of surgical volume reduction therapy (LVRS) and BLVR on lung and chest wall physiology will assist physicians in selecting an optimal approach for patients. OBJECTIVES: Determine whether LVRS adversely affects lung or chest wall physiology at 3-month follow-up relative to BLVR in an experimental model of sheep emphysema. METHODS: Twelve mixed-breed sheep were treated with papain to produce experimental emphysema, and were divided into control, LVRS, and BLVR treatment groups. Lung and chest wall impedance was measured at 0, 5, and 10 cm H2O positive end-expiratory pressure at baseline and 3-month follow-up. RESULTS: Emphysema was associated with increased airway resistance, decreased lung tissue resistance and elastance, and increased chest wall tissue resistance. Following treatment, equivalent increases in lung elastance occurred in the LVRS and BLVR groups compared to controls. LVRS did not adversely affect chest wall impedance despite causing extensive pleural scarring. CONCLUSIONS: (1) Experimental emphysema following prolonged papain exposure progresses after cessation of treatment. (2) BLVR and LVRS produced equivalent lung and chest wall impedance responses at 3-month follow-up. (3) LVRS did not adversely affect chest wall impedance despite being associated with extensive pleural scarring.

Animals↗