E12.5 pancreatic bud-derived cells are detected in recipient pancreata after intraplacental transplantation, but Pdx1-deficient recipients lack a macroscopically detectable pancreas.

The behavior of embryonic pancreatic bud-derived cells after intraplacental transplantation (IPT) into non-knockout versus Pdx1-deficient embryonic recipient contexts remains unclear. Here, we used IPT to compare the fate of dissociated E12.5 mouse pancreatic bud-derived cells in non-knockout recipients retaining an endogenous pancreatic developmental field and Pdx1-deficient mouse recipients. In a subset of non-knockout hosts, donor-derived cells were detected within endocrine, acinar, and ductal compartments, indicating donor-cell localization within pancreatic tissue compartments after transplantation. In contrast, grossly examined Pdx1-deficient recipients did not form macroscopically detectable organized pancreatic tissue. Some KO recipients in a serum-insulin endpoint cohort showed detectable circulating insulin. In a separate survival/blood-glucose cohort, IPT KO recipients showed transient postnatal increases in blood glucose followed by progressive hypoglycemia; survival and overall physiology were not normalized. Donor-cell localization in Pdx1-deficient recipients was not determined in this study. Thus, under the present donor-preparation and IPT conditions, E12.5 pancreatic bud-derived cells were detected within pancreatic tissue compartments in a subset of non-KO recipients but did not form macroscopically detectable organized pancreatic tissue in Pdx1-deficient recipients. Separately, analysis of published single-cell RNA-sequencing datasets, together with flow-cytometric validation, supported EPCAM as a reporter-independent epithelial enrichment marker that captures a large fraction of Pdx1-expressing epithelial cells in the E12.5 pancreatic bud. These parallel findings show that transplantation outcome differed between non-KO recipients retaining an endogenous pancreatic field and Pdx1-deficient recipients under the present IPT conditions and also support a practical strategy for enriching embryonic pancreatic epithelial fractions containing Pdx1-expressing cells.