ArticleScientific reports2026
E12.5 pancreatic bud-derived cells are detected in recipient pancreata after intraplacental transplantation, but Pdx1-deficient recipients lack a macroscopically detectable pancreas.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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