| First Author | Teitelman G | Year | 1998 |
| Journal | J Neurobiol | Volume | 34 |
| Issue | 4 | Pages | 304-18 |
| PubMed ID | 9514521 | Mgi Jnum | J:116956 |
| Mgi Id | MGI:3695262 | Doi | 10.1002/(sici)1097-4695(199803)34:4<304::aid-neu2>3.0.co;2-a |
| Citation | Teitelman G, et al. (1998) Islet injury induces neurotrophin expression in pancreatic cells and reactive gliosis of peri-islet Schwann cells. J Neurobiol 34(4):304-18 |
| abstractText | Pancreatic islets are enveloped by a sheath of Schwann cells, the glial cells of the peripheral nervous system (PNS). The fact that Schwann cells of the PNS become reactive and express nerve growth factor (NGF) and other growth factors following axotomy suggested the possibility that peri-islet Schwann cells could become activated by islet injury. To test this hypothesis, we examined two animal models of islet injury. The first model was mice and rats injected with streptozotocin (SZ), a specific beta-cell toxin. The second model was NOD mice, a strain in which beta cells are deleted by an autoimmune process. We found that peri-islet Schwann cells became reactive following islet injury and began to express increased levels of NGF and the neurotrophin receptor p75. Lesions to the pancreas also markedly induced NGF expression by exocrine and endocrine cells. Neurotrophin expression was not unique to adult tissues since pancreatic cells transiently expressed p75, the NGF receptor Trk A, and NGF during development. These observations suggest that NGF could play an important role in pancreas during embryogenesis and in processes leading to repair following islet injury in adults. |
