TY - JOUR
T1 - Expression of nerve growth factor in human pancreatic β cells
AU - Vidaltamayo, Román
AU - Mery, Carlos M.
AU - Ángeles-Ángeles, Arturo
AU - Robles-Díaz, Guillermo
AU - Hiriart, Marcia
N1 - Funding Information:
We are specially thankful to Carol Deutsch and Alvaro Caso for discussion and proof-correction of the manuscript, and to Tatiana Fiordelisio-Coll for discussion of methodology. We are also thankful to Carmen Sánchez-Soto for technical assistance in the laboratory. This work was supported by CONACyT (Consejo Nacional de Ciencia y Tecnología) 31740-N and DGAPA (Dirección General de Asuntos del Personal Académico) IN211800 grants.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2003/9/1
Y1 - 2003/9/1
N2 - Nerve growth factor (NGF) is an important modulator of rat pancreatic β-cell physiology in vitro. In this study, we analysed the expression of NGF, TrkA and insulin in human pancreatic islets from normal, ductal adenocarcinoma and insulinoma-afflicted samples, using double immunofluorescent labelling and confocal microscopy. We found that in normal human pancreas, insulin and NGF are co-expressed in β cells. Moreover, similar to previous observations in rat, the high affinity NGF receptor TrkA is also expressed in β cells. Pancreatic β cells in normal islets from adenocarcinoma and mucinous cystadenocarcinoma patients also expressed NGF. In 2 out of 15 exocrine tumour samples, NGF was detected also in the tissue surrounding the islets, while 2 out of 13 adenocarcinoma tumours expressed this growth factor. In five insulinoma samples, we observed weaker immunofluorescent labelling of insulin and NGF in the neoplastic tissue, compared to the islets not afflicted by the tumour, which may be a consequence of increased hormone secretion rate. We demonstrate that human β cells express TrkA and NGF. These findings are consistent with the hypothesis that NGF modulates insulin secretion through a paracrine/autocrine loop, similar to the one observed in cultured rat β cells.
AB - Nerve growth factor (NGF) is an important modulator of rat pancreatic β-cell physiology in vitro. In this study, we analysed the expression of NGF, TrkA and insulin in human pancreatic islets from normal, ductal adenocarcinoma and insulinoma-afflicted samples, using double immunofluorescent labelling and confocal microscopy. We found that in normal human pancreas, insulin and NGF are co-expressed in β cells. Moreover, similar to previous observations in rat, the high affinity NGF receptor TrkA is also expressed in β cells. Pancreatic β cells in normal islets from adenocarcinoma and mucinous cystadenocarcinoma patients also expressed NGF. In 2 out of 15 exocrine tumour samples, NGF was detected also in the tissue surrounding the islets, while 2 out of 13 adenocarcinoma tumours expressed this growth factor. In five insulinoma samples, we observed weaker immunofluorescent labelling of insulin and NGF in the neoplastic tissue, compared to the islets not afflicted by the tumour, which may be a consequence of increased hormone secretion rate. We demonstrate that human β cells express TrkA and NGF. These findings are consistent with the hypothesis that NGF modulates insulin secretion through a paracrine/autocrine loop, similar to the one observed in cultured rat β cells.
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U2 - 10.1080/08977190310001629566
DO - 10.1080/08977190310001629566
M3 - Article
SN - 0897-7194
VL - 21
SP - 103
EP - 107
JO - Growth Factors
JF - Growth Factors
IS - 3-4
ER -