title: Islet injury induces neurotrophin expression in pancreatic cells and reactive gliosis of peri-islet Schwann cells.
abstract: 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.
authors.affiliation: Department of Anatomy and Cell Biology, State University of New York Health Science Center at Brooklyn 11203, USA.
authors.forename: G
authors.initials: G
authors.lastname: Teitelman
authors.forename: Y
authors.initials: Y
authors.lastname: Guz
authors.forename: S
authors.initials: S
authors.lastname: Ivkovic
authors.forename: M
authors.initials: M
authors.lastname: Ehrlich
mesh_terms: D000818:Animals; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005911:Gliosis / Q000378:metabolism / Q000473:pathology*; D007515:Islets of Langerhans / Q000166:cytology / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D016688:Mice, Inbred NOD; D008820:Mice, Obese; D009414:Nerve Growth Factors / Q000096:biosynthesis* / Q000378:metabolism; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology; D010179:Pancreas / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases / Q000096:biosynthesis; D020800:Receptor, Nerve Growth Factor; D020917:Receptor, trkA; D017475:Receptors, Nerve Growth Factor / Q000032:analysis / Q000096:biosynthesis; D012583:Schwann Cells / Q000473:pathology*; D013311:Streptozocin / Q000494:pharmacology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D011518:Proto-Oncogene Proteins; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D013311:Streptozocin; D020794:Receptor Protein-Tyrosine Kinases; D020917:Receptor, trkA