| First Author | Nivlet L | Year | 2016 |
| Journal | J Mol Endocrinol | Volume | 56 |
| Issue | 2 | Pages | 77-90 |
| PubMed ID | 26576643 | Mgi Jnum | J:321242 |
| Mgi Id | MGI:6882724 | Doi | 10.1530/JME-15-0213 |
| Citation | Nivlet L, et al. (2016) Expression and functional studies of the GDNF family receptor alpha 3 in the pancreas. J Mol Endocrinol 56(2):77-90 |
| abstractText | The generation of therapeutic beta-cells from human pluripotent stem cells relies on the identification of growth factors that faithfully mimic pancreatic beta-cell development in vitro. In this context, the aim of the study was to determine the expression and function of the glial cell line derived neurotrophic factor receptor alpha 3 (GFRalpha3) and its ligand artemin (Artn) in islet cell development and function. GFRalpha3 and Artn expression were characterized by in situ hybridization, immunochemistry, and qRT-PCR. We used GFRalpha3-deficient mice to study GFRalpha3 function and generated transgenic mice overexpressing Artn in the embryonic pancreas to study Artn function. We found that GFRalpha3 is expressed at the surface of a subset of Ngn3-positive endocrine progenitors as well as of embryonic alpha- and beta-cells, while Artn is found in the pancreatic mesenchyme. Adult beta-cells lack GFRalpha3 but alpha-cells express the receptor. GFRalpha3 was also found in parasympathetic and sympathetic intra-islet neurons as well as in glial cells in the embryonic and adult pancreas. The loss of GFRalpha3 or overexpression of Artn has no impact on Ngn3 and islet cell formation and maintenance in the embryo. Islet organization and innervation as well as glucose homeostasis is normal in GFRalpha3-deficient mice suggesting functional redundancy. |
