Online Data Supplement and Databases

Using 3D spheroid models and spatial transcriptomics, we identified interactions between LAM-associated fibroblasts (LAMFs) and lymphatic endothelial cells (LECs) as contributors to Lymphangioleiomyomatosis pathogenesis, both responding to altered secretions driven by TSC2 mutations in LAM-cells, with bFGF, VEGF-A, and PDGFRB emerging as multikinase-sensitive factors and potential therapeutic targets to prevent LAMF invasion and LEC interaction.