Linda Clerch, Ph.D.

Professor, Department of Pediatrics
Lung Biology Laboratory

• B.A., Biology, Clark University
• M.S., Biochemistry, University of Miami
• Ph.D., Biochemistry and Molecular Biology, University of Miami

Contact Information:

Lung Biology Laboratory Georgetown University Medical Center Box 571481 Preclinical Science Building, Room GM12 3900 Reservoir Road, NW Washington, DC 20057 T: 202-687-4984 F: 202-687-8538 Contact Information

Our research is centered on understanding the regulation of lung gene expression during normal development, impaired lung growth, and lung repair/regeneration. Two major areas of focus are:

1. Prevention of oxidative damage to the lung in clinical situations where high oxygen concentration is used in therapy. In children this includes premature birth when the lung's antioxidant capacity is still undeveloped. Although surfactant therapy has been wonderful in reducing the incidence of respiratory distress syndrome, bronchopulmonary dysplasia (BDP) is on the rise in prematurely born infants and oxygen therapy is one of the main components involved in the pathogenesis of BPD. This work is centered on the effect of hyperoxia and the role RNA-binding proteins and microRNAs as regulators of post-transcriptional regulation in the developing mouse lung.
2. Identification of genes involved in the formation or regeneration of lung by the use of microarray profiling. In neonatal mice, this work is being done by comparing gene and microRNA expression during normal lung development, impaired development (neonatal mice treated with dexamethasone) and rescue from blocked development (treatment with all trans retinoic acid). In adult mice, this work is being done by gene expression profiling in the lungs of control mice, elastase-induced emphysematous mice, and mice undergoing lung regeneration (treatment with all trans retinoic acid). Small interfering RNA (siRNA) technology will be used to examine the function and significance of candidate genes.

We believe that molecular mechanisms revealed in the above mentioned animal models will translate to novel therapies for humans needing remediation for too few alveoli; for example, premature infants who have diminished alveolarization due to complications from BPD, and adults with too few alveoli due to the various causes of alveolar destruction, for example emphysema, anorexia nervosa, diffuse viral infections, and interstitial fibrosis.

Representative Publications:

• Hoffman, E.P., Wang, Y., Massaro, D., Massaro, G., and Clerch, L. (2004) Expression profiling as a tool for diagnosis and pathway discovery: experimental design and technical considerations. Lung Development and Regeneration, Marcel Dekker, Inc, New York, NY. 197-216.
• Clerch, L.B., Baras A.S., Massaro G.D., Hoffman E.P., and Massaro D. (2004) DNA microarray analysis of neonatal mouse lung connects regulation of KDR with dexamethasone-induced inhibition of alveolar formation. American Journal of Physiology, 286:L411-L419.
• Massaro, D. Massaro, G.D., and Clerch, L.B. (2004) Noninvasive delivery of small inhibitory RNA and other reagents to pulmonary alveoli in mice. American Journal of Physiology, 287: L1066-L1070.

More Publications at PubMed