The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Carmona Rita - One of the best experts on this subject based on the ideXlab platform.
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Role of the Wilms' tumor suppressor gene Wt1 in Pancreatic development
Wiley, 2018Co-Authors: Ariza Laura, Cañete Ana, Rojas Anabel, Muñoz-chápuli Ramón, Carmona RitaAbstract:The Wilms tumor suppressor gene (Wt1) encodes a transcription factor involved in the development of a number of organs, but the role played by Wt1 in Pancreatic development is unknown. The pancreas contains a population of Pancreatic stellate cells (PSC) very important for Pancreatic physiology. We described elsewhere that hepatic stellate cells originate from the WT1‐expressing liver mesothelium. Thus, we checked if the origin of PSCs was similar. WT1 expression is restricted to the Pancreatic mesothelium. Between embryonic day (E) 10.5 and E15.5, this mesothelium gives rise to mesenchymal cells that contribute to a major part of the PSC and other cell types including endothelial cells. Most WT1 systemic mutants show abnormal localization of the dorsal pancreas within the mesentery and intestinal malrotation by E14.0. Embryos with conditional deletion of WT1 between E9.5 and E12.5 showed normal dorsal Pancreatic Bud and intestine, but the number of acini in the ventral Bud was reduced approximately 30% by E16.5. Proliferation of acinar cells was reduced in WT1 systemic mutants, but Pancreatic differentiation was not impaired. Thus, mesothelial‐derived cells constitute an important subpopulation of Pancreatic mesodermal cells. WT1 expression is not essential for pancreas development, although it influences intestinal rotation and correct localization of the dorsal pancreas within the mesogastrium
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Role of the Wilms' tumor suppressor gene Wt1 in Pancreatic development
'Wiley', 2018Co-Authors: Ariza Laura, Cañete Ana, Rojas Anabel, Muñoz-chápuli Ramón, Carmona RitaAbstract:The Wilms tumor suppressor gene (Wt1) encodes a transcription factor involved in the development of a number of organs, but the role played by Wt1 in Pancreatic development is unknown. The pancreas contains a population of Pancreatic stellate cells (PSC) very important for Pancreatic physiology. We described elsewhere that hepatic stellate cells originate from the WT1‐expressing liver mesothelium. Thus, we checked if the origin of PSCs was similar. WT1 expression is restricted to the Pancreatic mesothelium. Between embryonic day (E) 10.5 and E15.5, this mesothelium gives rise to mesenchymal cells that contribute to a major part of the PSC and other cell types including endothelial cells. Most WT1 systemic mutants show abnormal localization of the dorsal pancreas within the mesentery and intestinal malrotation by E14.0. Embryos with conditional deletion of WT1 between E9.5 and E12.5 showed normal dorsal Pancreatic Bud and intestine, but the number of acini in the ventral Bud was reduced approximately 30% by E16.5. Proliferation of acinar cells was reduced in WT1 systemic mutants, but Pancreatic differentiation was not impaired. Thus, mesothelial‐derived cells constitute an important subpopulation of Pancreatic mesodermal cells. WT1 expression is not essential for pancreas development, although it influences intestinal rotation and correct localization of the dorsal pancreas within the mesogastrium.Spanish Ministry of Economy and Competitiveness . Grant Number: BFU2014‐52299‐P Instituto de Salud Carlos III‐TERCEL . Grant Number: RD12/0019‐0022 Junta de Andalucía . Grant Number: P11‐CTS‐07564Peer reviewe
Edward Passaro - One of the best experts on this subject based on the ideXlab platform.
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Pancreatic polypeptide immunoreactivity in sporadic gastrinoma: relationship to intraabdominal location.
Pancreas, 1995Co-Authors: Thomas J. Howard, Mark P. Sawicki, Klaus J. Lewin, Barbara Steel, Belur S. Bhagavan, Oscar W. Cummings, Edward PassaroAbstract:Sporadic gastrinoma is a Pancreatic endocrine tumor whose ontogeny is unknown. The anatomic area where the vast majority of sporadic gastrinomas is found (Pancreatic head region) corresponds topographically to the area traversed embryologically by the ventral Pancreatic Bud. Pancreatic polypeptide (PP), a 36-amino acid hormone, is secreted by Pancreatic endocrine cells derived almost exclusively from the ventral Pancreatic Bud and is proposed as a marker for ventral Bud derivation. Based on these observations we postulate that sporadic gastrinomas, found around the head of the pancreas, are derived from ventral Bud tissue and should display a high incidence of PP immunoreactivity. Overall, we found PP immunoreactivity in 7 of 14 (50%) gastrinomas. Of those tumors located to the right of the superior mesenteric artery (SMA) (around the head of the pancreas), seven of nine (78%) contained PP, whereas no gastrinoma to the left of the SMA (n = 5) contained PP (p = 0.021; Fisher exact test). Only one other Pancreatic endocrine or exocrine tumor, a glucagonoma located to the left of the SMA, stained positively for PP. We conclude that sporadic gastrinomas found around the head of the pancreas (to the right of the SMA) have a high incidence of PP immunoreactivity. These findings are consistent with our hypothesis that sporadic gastrinomas are derived from the ventral Pancreatic Bud.
Francesco Argenton - One of the best experts on this subject based on the ideXlab platform.
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Function and regulation of zebrafish nkx2.2a during development of Pancreatic islet and ducts
Developmental biology, 2007Co-Authors: Stefan Pauls, Elisabetta Zecchin, Natascia Tiso, Marino Bortolussi, Francesco ArgentonAbstract:In the mouse Nkx2.2 is expressed in the entire Pancreatic anlage. Nevertheless, absence of Nkx2.2 only perturbs the development of endocrine cell types, notably beta-cells which are completely absent. In order to test the possibility that Nkx2.2 might fulfil additional functions during pancreas development we analysed its zebrafish homologue nkx2.2a using gene targeting and GFP-transgenic fish lines. Our results suggest similar roles for nkx2.2a and Nkx2.2 during the development of the endocrine pancreas. Morpholino-based knock-down of nkx2.2a leads to a reduction of alpha- and beta-cell number and an increase of ghrelin-producing cells but, as in mice, does not affect delta-cells. Moreover, like in the mouse, two spatially distinct promoters regulate expression of nkx2.2a in precursors and differentiated islet cells. In addition we found that in zebrafish nkx2.2a is also expressed in the anterior Pancreatic Bud and, later, in the differentiated Pancreatic ducts. A nkx2.2a-transgenic line in which Pancreatic GFP expression is restricted to the Pancreatic ducts revealed that single GFP-positive cells leave the anterior Pancreatic Bud and move towards the islet where they form intercellular connections between each other. Subsequently, these cells generate the branched network of the larval Pancreatic ducts. Morpholinos that block nkx2.2a function also lead to the absence of the Pancreatic ducts. We observed the same phenotype in ptf1a-morphants that are additionally characterized by a reduced number of nkx2.2a-positive duct precursors. Whereas important details of the molecular program leading to the differentiation of endocrine cell types are conserved between mammals and zebrafish, our results reveal a new function for nkx2.2a in the development of the Pancreatic ducts.
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Genomes & Developmental Control Function and regulation of zebrafish nkx2.2a during development of Pancreatic islet and ducts
2007Co-Authors: Stefan Pauls, Elisabetta Zecchin, Natascia Tiso, Marino Bortolussi, Francesco ArgentonAbstract:In the mouse Nkx2.2 is expressed in the entire Pancreatic anlage. Nevertheless, absence of Nkx2.2 only perturbs the development of endocrine cell types, notably beta-cells which are completely absent. In order to test the possibility that Nkx2.2 might fulfil additional functions during pancreas development we analysed its zebrafish homologue nkx2.2a using gene targeting and GFP-transgenic fish lines. Our results suggest similar roles for nkx2.2a and Nkx2.2 during the development of the endocrine pancreas. Morpholino-based knock-down of nkx2.2a leads to a reduction of alpha- and beta-cell number and an increase of ghrelin-producing cells but, as in mice, does not affect delta-cells. Moreover, like in the mouse, two spatially distinct promoters regulate expression of nkx2.2a in precursors and differentiated islet cells. In addition we found that in zebrafish nkx2.2a is also expressed in the anterior Pancreatic Bud and, later, in the differentiated Pancreatic ducts. A nkx2.2a-transgenic line in which Pancreatic GFP expression is restricted to the Pancreatic ducts revealed that single GFP-positive cells leave the anterior Pancreatic Bud and move towards the islet where they form intercellular connections between each other. Subsequently, these cells generate the branched network of the larval Pancreatic ducts. Morpholinos that block nkx2.2a function also lead to the absence of the Pancreatic ducts. We observed the same phenotype in ptf1a-morphants that are additionally characterized by a reduced number of nkx2.2a-positive duct precursors. Whereas important details of the molecular program leading to the differentiation of endocrine cell types are conserved between mammals and zebrafish, our results reveal a new function for nkx2.2a in the development of the Pancreatic ducts.
Beverley Kramer - One of the best experts on this subject based on the ideXlab platform.
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EXOGENOUS ACTIVIN INCREASES THE PROPORTION OF INSULIN CELLS IN THE DEVELOPING CHICK PANCREAS IN CULTURE
Cell biology international, 2002Co-Authors: Clem B. Penny, Beverley KramerAbstract:As activin is believed to be a key signalling factor during early Pancreatic development, its influence on the proliferation and/or determination of insulin cells in the developing chick dorsal Pancreatic Bud was investigated. Dorsal Pancreatic Buds of 5-day-old chick embryos were explanted on to Matrigel and cultured in serum-free medium (Ham's F12.ITS), to which 1 or 10 ng/ml activin was added. After 7 days in culture, the explants were processed for immunocytochemistry and the insulin-positive cells were scored and expressed as a proportion of the sum of insulin and glucagon cells. When compared to the control cultures (Hams F12.ITS alone), activin treatment resulted in respective increases in the proportion of insulin cells of 1.6 and 1.9 fold. It is suggested that activin treatment favours differentiation of the insulin cell pathway relative to glucagon cells.
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Regulation of embryonic chick insulin cells: effect of retinoic acid and insulin-like growth factor 1.
Cells tissues organs, 2001Co-Authors: Beverley Kramer, Clem B. PennyAbstract:We are interested in the regulation of early Pancreatic differentiation, particularly with regard to factors that enhance insulin cell proliferation. Both retinoic acid and insulin-like growth factor 1 (IGF-1) are known to be important in the proliferation and differentiation of insulin cells. Individually, they have the ability to increase the proportion of insulin cells when added to cultures of chick dorsal Pancreatic Buds. The aim of this study was to define the action of retinoic acid (RA) in combination with IGF-1 on the proportion of insulin cells. The dorsal Pancreatic Bud of 5-day-old chick embryos was excised and the endodermal component, with minimal adherent mesenchyme, was explanted onto Matrigel. RA (10(-6) M) and IGF-1 (50 ng/ml) were added to Ham's F12 culture medium containing transferrin (5 microg/ml) and selenium (10(-10) M) (F12.TS). Control explants were cultured in F12.TS alone or in F12.TS containing dimethyl sulphoxide (DMSO) [F12.TS (DMSO)]. After 7 days in culture, insulin and glucagon cells were localized immunocytochemically; numbers of insulin cells were expressed as a percentage of insulin plus glucagon cell counts. Addition of RA plus IGF-1 to the medium increased the proportion of insulin cells markedly (23.43%) compared with the proportions in control explants (11.3% with F12.TS (DMSO), 13.2% with F12.TS). This increase represents a more than twofold increase in the proportion of insulin cells over that of control explants.
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The effect of retinoic acid on the proportion of insulin cells in the developing chick pancreas
In Vitro Cellular & Developmental Biology - Animal, 2000Co-Authors: Clem Penny, Beverley KramerAbstract:We assessed the potential role of all- trans -retinoic acid on the developing chick pancreas, specifically with regard to the proportions of insulin cells. The endodermal component of the dorsal Pancreatic Bud of 5-d-old chick embryos was cultured on Matrigel. Retinoic acid (10^−6 or 10^−5 M ) was added to a standard serum-free medium, Ham's F12 containing insulin, transferrin and selenium (F12.ITS). Control grafts were cultured in F12.ITS alone or in F12.ITS with DMSO (the diluent for retinoic acid). After 7 d the explants were retrieved, freeze-dried, vapor-fixed, and embedded in resin. Endocrine cell types were identified by immunocytochemistry. The numbers of insulin cells were expressed as a proportion of the sum of insulin plus glucagon cells. Retinoic acid had a dose-related effect; the proportion of insulin cells in explants treated with the lower dose of retinoic acid (10^−6 M ) was more than twice the proportion of insulin cells in explants treated with the higher dose (10^−5 M ) of retinoic acid and more than three times that of the control grafts.
Thomas J. Howard - One of the best experts on this subject based on the ideXlab platform.
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The origin of sporadic gastrinomas within the gastrinoma triangle: a theory
Archives of surgery (Chicago Ill. : 1960), 1998Co-Authors: E. Passaro, Thomas J. Howard, Mark P. Sawicki, Philip C. Watt, Bruce E. StabileAbstract:Sporadic gastrinomas are found predominantly within the gastrinoma triangle (85%), frequently within lymph nodes in the triangle (40%) and often multiple (40%). In addition, they are homologous with Pancreatic polypeptidomas and express Pancreatic polypeptide. We hypothesized that, if gastrinomas were of ventral Pancreatic Bud origin, several (7) predictions could be made. The data from the investigation of these predictions have supported the theory. We postulate that sporadic gastrinomas in the triangle arise from stem cells from the ventral Pancreatic Bud that become dispersed and incorporated into lymph tissue and the duodenal wall during the ventral Bud's embryonic dorsal rotation within the area of the triangle.
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Pancreatic polypeptide immunoreactivity in sporadic gastrinoma: relationship to intraabdominal location.
Pancreas, 1995Co-Authors: Thomas J. Howard, Mark P. Sawicki, Klaus J. Lewin, Barbara Steel, Belur S. Bhagavan, Oscar W. Cummings, Edward PassaroAbstract:Sporadic gastrinoma is a Pancreatic endocrine tumor whose ontogeny is unknown. The anatomic area where the vast majority of sporadic gastrinomas is found (Pancreatic head region) corresponds topographically to the area traversed embryologically by the ventral Pancreatic Bud. Pancreatic polypeptide (PP), a 36-amino acid hormone, is secreted by Pancreatic endocrine cells derived almost exclusively from the ventral Pancreatic Bud and is proposed as a marker for ventral Bud derivation. Based on these observations we postulate that sporadic gastrinomas, found around the head of the pancreas, are derived from ventral Bud tissue and should display a high incidence of PP immunoreactivity. Overall, we found PP immunoreactivity in 7 of 14 (50%) gastrinomas. Of those tumors located to the right of the superior mesenteric artery (SMA) (around the head of the pancreas), seven of nine (78%) contained PP, whereas no gastrinoma to the left of the SMA (n = 5) contained PP (p = 0.021; Fisher exact test). Only one other Pancreatic endocrine or exocrine tumor, a glucagonoma located to the left of the SMA, stained positively for PP. We conclude that sporadic gastrinomas found around the head of the pancreas (to the right of the SMA) have a high incidence of PP immunoreactivity. These findings are consistent with our hypothesis that sporadic gastrinomas are derived from the ventral Pancreatic Bud.
