Date: 6 November 2026 (Friday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 304, 3/F, William M.W. Mong Block, 21 Sassoon Road 
Host: Professor Mu He

David M. Ornitz, MD, PhD, is the Alumni Endowed Professor of Developmental Biology at Washington University School of Medicine in St. Louis, USA. He received his MD and PhD from the University of Washington and completed postdoctoral training at Harvard Medical School. During his early career, he pioneered genetic approaches to modeling human diseases in mice and discovered the essential role of heparan sulfate proteoglycans in Fibroblast Growth Factor (FGF) signaling.

Dr. Ornitz joined the faculty at Washington University in 1991. His research has focused on understanding the functions of FGF signaling in organ development, physiology, tissue regeneration, and disease, with major contributions to pulmonary, cardiovascular, and skeletal biology. He is an elected Fellow of the American Association for the Advancement of Science (AAAS) and the American Association for Anatomy (AAA).

Alveologenesis expands lung gas-exchange surface area through formation of elastin-rich septal ridges and requires coordinated development of secondary crest myofibroblasts (MyoFB) and matrix fibroblasts (MatFB). We identify fibroblast growth factor 18 (FGF18) as a paracrine signal that coordinates these mesenchymal populations during neonatal lung development. Conditional inactivation of Fgf18 in Fgf18-expressing cells impaired secondary septation and elastin organization, altered MAPK and AKT signaling, accelerated MyoFB maturation, reduced mesenchymal proliferation, and expanded a MatFB-associated double-positive cell (DPC) state co-expressing MyoFB and MatFB gene programs. DPCs were normally enriched early in alveologenesis and declined with maturation but persisted after Fgf18loss and neonatal hyperoxia. Analysis of human bronchopulmonary dysplasia (BPD) identified expansion of an analogous MEOX2-ACTA2 DPC population, altered downstream FGF signaling, and reduced elastin expression. Together, these findings define FGF18 as a regulator of fibroblast maturation and state transitions during alveologenesis and link impaired FGF-dependent mesenchymal signaling to persistence of a transitional fibroblast state in experimental lung injury and human BPD.

All are welcome.