PYY in developing murine islet cells: comparisons to development of islet                hormones, NPY, and BrdU incorporation.

Jackerott, Malene; Øster, Anne; Larsson, Lars‐Inge

doi:10.1177/44.8.8756753

Cited by 69 publications

(63 citation statements)

References 10 publications

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“…The co-localization of PYY and glucagon agrees with findings by Ali-Rachedi et al (12) in the human fetal pancreas and by Upchurch et al (11) and Jackerott et al (19) in mice. Co-localization of PYY and glucagonrelated peptides has also been reported in adult human intestinal mucosa.…”

Section: Journal Of Endocrinology (1999) 141supporting

confidence: 81%

Co-localization of neuroendocrine hormones in the human fetal pancreas

Portela-Gomes

Johansson²,

Olding³

et al. 1999

European Journal of Endocrinology

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Objective and Design: Co-localization of the four major pancreatic hormones, and also of islet amyloid polypeptide (IAPP), peptide tyrosine tyrosine (PYY), secretin and neurotensin, has been studied in the endocrine pancreas of human fetuses at 16, 18 and 22 weeks of gestation. Methods: Double and triple immunofluorescence stainings have been used. Results: All three fetal pancreata contained cells that showed insulin, glucagon, somatostatin, pancreatic polypeptide (PP), IAPP, secretin and PYY immunoreactivity. Neurotensin cells were found in the youngest fetus and gastric inhibitory polypeptide (GIP) in the two older fetuses. Colocalization of two hormones occurred in most of the endocrine cell types in the three fetuses examined, but three hormones occurred in only a few cells and especially in the youngest fetus. Somatostatin cells were the only cell type which was largely monohormonal. Our findings showed that there are two different co-localization patterns: insulin was co-localized mainly with IAPP and glucagon, while secretin and PYY occurred together with glucagon and PP. Conclusions: These data are the first to describe secretin and neurotensin in the fetal pancreas. Two different co-localization patterns could be distinguished: insulin, IAPP and glucagon, and glucagon, secretin, PP and PYY.

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Section: Journal Of Endocrinology (1999) 141supporting

confidence: 81%

Co-localization of neuroendocrine hormones in the human fetal pancreas

Portela-Gomes

Johansson²,

Olding³

et al. 1999

European Journal of Endocrinology

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“…1D). As previously described (Alpert et al 1988, Jackerott et al 1996, at that stage, the insulin-expressing cells co-express glucagon (compare Fig. 1C and D).…”

Section: Immunostaining Analysis Of Trk-a Expression During Pancreatimentioning

confidence: 81%

“…Using immunochemistry, we found these first insulin-positive cells at E11 within the pancreatic epithelial mass. At this stage, as described previously (Alpert et al 1988, Jackerott et al 1996, all insulin-expressing cells stained positive for glucagon. Double immunostaining with anti-Trk-A (763) and either anti-glucagon or antiinsulin antibodies indicates that the vast majority of these early endocrine cells co-express the Trk-A protein.…”

Section: Discussionmentioning

confidence: 99%

Expression of nerve growth factor and its high-affinity receptor Trk-A in the rat pancreas during embryonic and fetal life

Miralles¹,

Philippe²,

Czernichow³

et al. 1998

Journal of Endocrinology

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The expression of functional receptors for nerve growth factor in insulin-producing cell lines grown in vitro has recently been demonstrated. The possible importance of signals transduced via these receptors in the control of islet maturation has been proposed based on data obtained using an in vitro culture system. To further support this hypothesis, we have studied the expression of Trk-A, the high-affinity receptor for NGF, in vivo during the embryonic and fetal development of the rat pancreas. We have also examined the expression of NGF during the same period. Immunohistological analysis shows that at embryonic day 11 (E11), Trk-A is expressed by the epithelial cells of the presumptive pancreas. The few pancreatic endocrine cells present at that stage express Trk-A. At E12 and E16, Trk-A expression was detected in the developing ductal network. The endocrine cells located in the ducts express Trk-A while those that have migrated into the surrounding mesenchyme now stain negative for Trk-A. By E20, Trk-A expression by ductal cells has considerably decreased and can be detected only in small ducts closely associated with islet-like structures. These islet-like structures stain negative for Trk-A. After birth, insulin-positive cells arranged into islets re-express Trk-A. During the same period, NGF mRNA is found to be expressed in the developing pancreas. The expression of Trk-A and its ligand NGF in the pancreas during embryonic and fetal life suggests that NGF and its receptor could play an important role in the development of the pancreas.

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“…Somatostatin and PP mRNA are also detected at this time (Herrera et al 1991, Gittes & Rutter 1992. However, the proteins only appear from E15·5 and E16 respectively (Teitelman et al 1993, Jackerott et al 1996. In mice, islets are formed properly only within a few days of birth after a secondary wave of beta cell differentiation (Slack 1995).…”

Section: Discussionmentioning

confidence: 99%

Beta cell differentiation during early human pancreas development

Piper

Brickwood²,

Turnpenny³

et al. 2004

Journal of Endocrinology

270

244

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Understanding gene expression profiles during early human pancreas development is limited by comparison to studies in rodents. In this study, from the inception of pancreatic formation, embryonic pancreatic epithelial cells, approximately half of which were proliferative, expressed nuclear PDX1 and cytoplasmic CK19. Later, in the fetal pancreas, insulin was the most abundant hormone detected during the first trimester in largely nonproliferative cells. At sequential stages of early fetal development, as the number of insulin-positive cell clusters increased, the detection of CK19 in these cells diminished. PDX1 remained expressed in fetal beta cells. Vascular structures were present within the loose stroma surrounding pancreatic epithelial cells during embryogenesis. At 10 weeks post-conception (w.p.c.), all clusters containing more than ten insulin-positive cells had developed an intimate relationship with these vessels, compared with the remainder of the developing pancreas. At 12-13 w.p.c., human fetal islets, penetrated by vasculature, contained cells independently immunoreactive for insulin, glucagon, somatostatin and pancreatic polypeptide (PP), coincident with the expression of maturity markers prohormone convertase 1/3 (PC1/3), islet amyloid polypeptide, Chromogranin A and, more weakly, GLUT2. These data support the function of fetal beta cells as true endocrine cells by the end of the first trimester of human pregnancy.

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PYY in developing murine islet cells: comparisons to development of islet hormones, NPY, and BrdU incorporation.

Cited by 69 publications

References 10 publications

Co-localization of neuroendocrine hormones in the human fetal pancreas

Co-localization of neuroendocrine hormones in the human fetal pancreas

Expression of nerve growth factor and its high-affinity receptor Trk-A in the rat pancreas during embryonic and fetal life

Beta cell differentiation during early human pancreas development

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