Retinoic acid signaling within pancreatic endocrine progenitors regulates mouse and human β cell specification.

ABSTRACT: Retinoic acid (RA) signaling is essential for multiple developmental processes, including appropriate pancreas formation from the foregut endoderm. RA is also required to generate pancreatic progenitors from human pluripotent stem cells. However, the role of RA signaling during endocrine specification has not been fully explored. In this study, we demonstrate that the disruption of RA signaling within the NEUROG3-expressing endocrine progenitor population impairs mouse β cell differentiation and induces ectopic expression of crucial δ cell genes, including somatostatin. In addition, the inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG3 induction impairs insulin expression. We further determine that RA-mediated regulation of endocrine cell differentia

SUBMITTER: Lorberbaum DS 

PROVIDER: S-EPMC7328135 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature