Bronchopulmonary Dysplasia (BPD)

Babies who are born prematurely or who experience respiratory problems shortly after birth are at risk for bronchopulmonary dysplasia (BPD), sometimes called chronic lung disease. Although most infants fully recover from BPD and have few long-term health problems as a result, BPD can be a serious condition requiring intensive medical care.

Investigators are identifying biomarkers associated with BPD in order to develop personalized therapies to prevent the disease and improve patient outcome. Collaboration within Nationwide Children’s Hospital and a unique relationship with the Antipartum Unit and the Labor and Delivery Unit at The Ohio State University Medical Center allows researchers to more easily identify eligible study participants and merge clinical and laboratory data.

Faculty and Staff Focused on BPD Research

Basic Science/Translational:

• Trent E. Tipple, MD
• Leif D. Nelin, MD
• Lynette K. Rogers, PhD
• Bernadette Chen, MD
• Fred Long, MD

Clinical/Translational Research:

• George Mandy, MD
• Edward Shepherd, MD
• Robert Castille, MD
• Kelly Susey, PT
• Melissa Hanin, OT

Latest Findings in BPD Research

The Role of Clara Cells in Acute Lung Injury
Increased innate immune responses can contribute to development of acute lung injury.  This study suggests the importance of Clara cells in the pathogenesis of LPS-induced acute lung injury.

Access an abstract of this study: Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Mouse Transformed Clara Cells. Cell Physiol Biochem. 2012;29(1-2):213-22.

cAMP May Inhibit Arginase Activity Related to Hypoxia
Arginase II has been shown to be involved in the hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (hPASMC.).  These data are the first to describe the inhibitory effect of cAMP on arginase activity, expression, and proliferation of hypoxic hPASMC.

Access an abstract of this study: Pharmacologic Agents Elevating cAMP Prevent Arginase II Expression and Proliferation of Pulmonary Artery Smooth Muscle Cells. Am J Respir Cell Mol Biol. 2012 Mar 23. [Epub ahead of print]

CAT Over-Expression Increases Nitric Oxide Production in Human Lung Cells
This study tested whether oxygen deprivation decreases expression of cationic amino acid transporters (CAT) and decreases L-arginine update, leading to decreased nitric oxide production in human lung cells.  This study suggests that CAT may represent a new therapeutic target for treating pulmonary hypertensive disorders.

Access an abstract of this study: Overexpression of cationic amino acid transporter-1 increases nitric oxide production in hypoxic human pulmonary microvascular endothelial cells. Clin Exp Pharmacol Physiol. 2011 Sep 16. doi: 10.1111/j.1440-1681.2011.05609.x. [Epub ahead of print] 

CAT Helps Control Lung Cell Growth Suppressed by Nitric Oxide
These data demonstrate that iNOS expression in lung endothelial cells decreases cell growth and production.  Preventing uptake of L-arginine in cells can help limit this decrease.  This study suggests that cationic amino acid transporter (CAT) activity may represent a new therapeutic target in inflammatory lung diseases characterized by nitric oxide overproduction.

Access an abstract of this study: Nitric oxide suppression of cellular proliferation depends on cationic amino acid transporter activity in cytokine-stimulated pulmonary endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2011 Apr;300(4):L596-604.  

Current BPD Research Grants

Lipoxin-Mediated Inflammatory Resolution in Newborn Hyperoxic Lung Injury, National Institutes of Health (Rodney Britt)

DHA Attenuates Inflammatory Responses through Altering RAGE Signaling, National Institutes of Health (Lynette Rogers)

Cationic Amino Acid Transporters and Lung NO Production, National Heart, Lung and Blood Institute, National Institutes of Health (Leif D. Nelin)

Lipoxin Receptor and Inflammatory Resolution in the Development of Bronchopulmonary Dysplasia, American Thoracic Society (Lynette K. Rogers)

Regulation of Lung Growth and Development by Thioredoxin Interacting Protein, National Institutes of Health, National Hearth, Lung, and Blood Institute (Trent E. Tipple)

miR-17~92 Cluster Expression in Bronchopulmonary Dysplasia, Richard P. & Marie R. Bremer Medical Research Fund and William H. Davis Endowment for Basic Medical Research and The Ohio State University Center for Clinical & Translational Science Pilot Program (Trent E. Tipple, MD)