I’m a biomedical researcher and director of the Division of Pulmonary Biology. My lab is interested in the normal developmental processes that build the lung and how such processes go awry during lung malformations, injury and tumorigenesis. I mainly focus on intercellular signaling and transcriptional control, using a combination of mouse genetics, single-cell genomics, three-dimensional (3D) imaging and artificial intelligence.

As genome sequencing has cataloged deoxyribonucleic acid (DNA) blueprints and the cell atlas endeavor is cataloging constituent cell populations of each organ, our view of lung biology is increasingly genome-wide with single-cell precision. This level of understanding is timely given the tremendous health and economic burden of lung diseases, including lung cancers, pediatric and chronic respiratory diseases and infections exacerbated by the COVID-19 pandemic.

Our research led to the publication of our findings that alveolar type 1 (AT1) cell-derived vascular endothelial growth factor A (VEGFA) is required to specify a previously unknown capillary endothelial cell population marked by Carbonic anhydrase 4 (CAR4), contrasting the conventional wisdom of the homogeneity of pulmonary capillaries; and CAR4+ endothelial cells, also known as capillary 2 (CAP2) or aerosol capillary (aCap) cells, have unique morphology, localization, and function in alveologenesis — with implications in bronchopulmonary dysplasia (BPD).

We also showed that canonical Wnt signaling components, including catenin beta-1 (CTNNB1) and the four T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors, are required to promote the progenitor program, as well as suppress premature alveolar differentiation and the aberrant gastrointestinal fate in SRY-Box Transcription Factor 9 (SOX9)+ progenitors. In addition, we showed that contrary to prior studies, the lung lineage transcription factor NK2 homeobox 1 (NKX2-1) is expressed by both AT1 and AT2 cells and is required for their specification and maintenance and that cell-type-specific cofactors, Yes-associated protein/transcriptional coactivator with PDZ-binding motif/TEA domain transcription factor (YAP/TAZ/TEAD) in AT1 cells, direct NKX2-1 to cell-type-specific binding sites. Additionally, we generated a tricolor cell biology reporter, dubbed Kaleidoscope, to conditionally express fluorescent fusion proteins to visualize microtubules, mitochondria and lysosomes in any cell type in any organ.

I was honored to give the Anita Kurmann Memorial Lecture (2023) and to receive the Paul E. Darlington Mentor Award (2022), the John P. McGovern Award for Outstanding Teaching (2021), the American Lung Association Innovation Award (2019), the MD Anderson Cyrus Scholar Award (2016), the March of Dimes Basil O’Connor Scholar Award (2015), the MD Anderson inaugural R. Lee Clark Fellow Award (2014) and the Jane Coffin Childs Memorial Fund for Medical Research (2007).

I’ve been a biomedical researcher for over 25 years and began working at Cincinnati Children’s in 2024.