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Fanconi anemia (FA) patients develop bone marrow (BM) failure or leukemia. One standard care for these devastating complications is hematopoietic stem cell transplantation. We identified a group of mesenchymal stromal cells (MSCs)‐derived metabolites, glycerophospholipids, and their endogenous inhibitor, 5‐(tetradecyloxy)−2‐furoic acid (TOFA), as regulators of donor hematopoietic stem and progenitor cells. We provided two pieces of evidence that TOFA could improve hematopoiesis‐supporting function of FA MSCs: (a) limiting‐dilution cobblestone area‐forming cell assay revealed that TOFA significantly increased cobblestone colonies in  Fanca−/−  or  Fancd2−/−  cocultures compared to untreated cocultures. (b) Competitive repopulating assay using output cells collected from cocultures showed that TOFA greatly alleviated the abnormal expansion of the donor myeloid (CD45.2+Gr1+Mac1+) compartment in both peripheral blood and BM of recipient mice transplanted with cells from  Fanca−/−  or  Fancd2−/−  cocultures. Furthermore, mechanistic studies identified Tlr4 signaling as the responsible pathway mediating the effect of glycerophospholipids. Thus, targeting glycerophospholipid biosynthesis in FA MSCs could be a therapeutic strategy to improve hematopoiesis and stem cell transplantation. S tem  C ells   2015;33:3382–3396

stem cells

Fanconi Anemia Mesenchymal Stromal Cells‐Derived Glycerophospholipids Skew Hematopoietic Stem Cell Differentiation Through Toll‐Like Receptor Signaling