| First Author | Tingstedt JE | Year | 1999 |
| Journal | J Histochem Cytochem | Volume | 47 |
| Issue | 8 | Pages | 973-80 |
| PubMed ID | 10424881 | Mgi Jnum | J:56760 |
| Mgi Id | MGI:1342390 | Doi | 10.1177/002215549904700801 |
| Citation | Tingstedt JE, et al. (1999) Gastric amylin expression. Cellular identity and lack of requirement for the homeobox protein PDX-1. A study in normal and PDX-1-deficient animals with a cautionary note on antiserum evaluation. J Histochem Cytochem 47(8):973-80 |
| abstractText | The gene encoding amylin is implicated in the generation of amyloid in the islets of Langerhans of diabetics and is believed to be regulated by the homeodomain transcription factor PDX-1. Although gastric mucosa also produces amylin, studies on its cellular site of production have yielded highly divergent results, localizing this peptide to either gastrin, serotonin, or somatostatin cells or to combinations thereof. Using region-specific amylin antisera in combination with reverse transcriptase-polymerase chain reaction, we now document that the majority of cells expressing amylin correspond to somatostatin cells. Only a small subpopulation of gastrin cells contained immunoreactive amylin. Studies of PDX-1-deficient mice, which fail to develop gastrin cells while possessing normal numbers of somatostatin cells, revealed no detectable change in gastric amylin expression. These data show that neither normal gastrin cell development nor PDX-1 expression is needed for gastric amylin expression. |
