Our previous studies showed human adipose-derived mesenchymal stem cells (ADSCs) produce an activity that stimulated wound healing in eardrum keratinocytes (hTMk)1. By regulating ADSCs in hypoxia (<0.1% O2), this wound healing stimulus was increased. To understand the molecular mechanism behind this paracrine activity of ADSCs on wound healing, we used a bioinformatics approach to determine ADSCs and hTMk transcriptome for secreted ligands and receptors. Primary ADSCs were cultured in ambient oxygen conditions (21%) or hypoxia for 48h without serum. hTMk were established under normoxic conditions. Conditioned media were collected from ADSCs to assess paracrine activity on hTMk proliferation and migration, and to quantify specific protein secretion using ELISA. Transcriptomic analysis of ADSCs and hTMk were assessed using RNAseq and bioinformatics. Transcripts differentially expressed (P-adj <0.05) between each primary hypoxic and normoxic ADSCs were filtered through databases to identify secreted ligands, and similarly for hTMk transcriptome to identify receptors. Both subsets were then matched to a FANTOM5 curated ligand-receptor pair database2 to establish the final list of ligand-receptor repertoires. Results show hypoxia in ADSC consistently up-regulated VEGFA more than 3 fold, with corresponding receptors expressed at mRNA level on the hTMk. This could potentially represent a previously unknown function in wound healing.