Relevant bibliographies by topics / Pancreatic differentiation

Academic literature on the topic 'Pancreatic differentiation'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Pancreatic differentiation"

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Mehta, Sheilendra, and George K. Gittes. "Pancreatic differentiation." Journal of Hepato-Biliary-Pancreatic Surgery 12, no. 3 (June 27, 2005): 208–17. http://dx.doi.org/10.1007/s00534-005-0981-4.

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Russ, Holger A., Limor Landsman, Christopher L. Moss, Roger Higdon, Renee L. Greer, Kelly Kaihara, Randy Salamon, Eugene Kolker, and Matthias Hebrok. "Dynamic Proteomic Analysis of Pancreatic Mesenchyme Reveals Novel Factors That Enhance Human Embryonic Stem Cell to Pancreatic Cell Differentiation." Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/6183562.

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Current approaches in human embryonic stem cell (hESC) to pancreatic beta cell differentiation have largely been based on knowledge gained from developmental studies of the epithelial pancreas, while the potential roles of other supporting tissue compartments have not been fully explored. One such tissue is the pancreatic mesenchyme that supports epithelial organogenesis throughout embryogenesis. We hypothesized that detailed characterization of the pancreatic mesenchyme might result in the identification of novel factors not used in current differentiation protocols. Supplementing existing hESC differentiation conditions with such factors might create a more comprehensive simulation of normal development in cell culture. To validate our hypothesis, we took advantage of a novel transgenic mouse model to isolate the pancreatic mesenchyme at distinct embryonic and postnatal stages for subsequent proteomic analysis. Refined sample preparation and analysis conditions across four embryonic and prenatal time points resulted in the identification of 21,498 peptides with high-confidence mapping to 1,502 proteins. Expression analysis of pancreata confirmed the presence of three potentially important factors in cell differentiation: Galectin-1 (LGALS1), Neuroplastin (NPTN), and the Lamininα-2 subunit (LAMA2). Two of the three factors (LGALS1 and LAMA2) increased expression of pancreatic progenitor transcript levels in a published hESC to beta cell differentiation protocol. In addition, LAMA2 partially blocks cell culture induced beta cell dedifferentiation. Summarily, we provide evidence that proteomic analysis of supporting tissues such as the pancreatic mesenchyme allows for the identification of potentially important factors guiding hESC to pancreas differentiation.
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Pour, P. M. "Cell Differentiation during Pancreatic Carcinogenesis." Scandinavian Journal of Gastroenterology 23, sup151 (January 1988): 123–30. http://dx.doi.org/10.3109/00365528809095924.

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Mehta, Sheilendra S., and George K. Gittes. "Extracellular control of pancreatic differentiation." Seminars in Pediatric Surgery 13, no. 1 (February 2004): 25–36. http://dx.doi.org/10.1053/j.sempedsurg.2003.09.005.

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Rao, M. Sambasiva, and Janardan K. Reddy. "Pancreatic Stem Cells: Differentiation Options." Stem Cell Reviews 1, no. 3 (2005): 265–72. http://dx.doi.org/10.1385/scr:1:3:265.

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Miettinen, P. J., M. Huotari, T. Koivisto, J. Ustinov, J. Palgi, S. Rasilainen, E. Lehtonen, J. Keski-Oja, and T. Otonkoski. "Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors." Development 127, no. 12 (June 15, 2000): 2617–27. http://dx.doi.org/10.1242/dev.127.12.2617.

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Pancreatic acini and islets are believed to differentiate from common ductal precursors through a process requiring various growth factors. Epidermal growth factor receptor (EGF-R) is expressed throughout the developing pancreas. We have analyzed here the pancreatic phenotype of EGF-R deficient (−/−) mice, which generally die from epithelial immaturity within the first postnatal week. The pancreata appeared macroscopically normal. The most striking feature of the EGF-R (−/−) islets was that instead of forming circular clusters, the islet cells were mainly located in streak-like structures directly associated with pancreatic ducts. Based on BrdU-labelling, proliferation of the neonatal EGF-R (−/−) beta-cells was significantly reduced (2.6+/−0.4 versus 5.8+/−0.9%, P<0.01) and the difference persisted even at 7–11 days of age. Analysis of embryonic pancreata revealed impaired branching morphogenesis and delayed islet cell differentiation in the EGF-R (−/−) mice. Islet development was analyzed further in organ cultures of E12.5 pancreata. The proportion of insulin-positive cells was significantly lower in the EGF-R (−/−) explants (27+/−6 versus 48+/−8%, P<0.01), indicating delayed differentiation of the beta cells. Branching of the epithelium into ducts was also impaired. Matrix metalloproteinase (MMP-2 and MMP-9) activity was reduced 20% in EGF-R (−/−) late-gestation pancreata, as measured by gelatinase assays. Furthermore, the levels of secreted plasminogen activator inhibitor-1 (PAI-1) were markedly higher, while no apparent differences were seen in the levels of active uPA and tPa between EGF-R (−/−) and wild-type pancreata. Our findings suggest that the perturbation of EGF-R-mediated signalling can lead to a generalized proliferation defect of the pancreatic epithelia associated with a delay in beta cell development and disturbed migration of the developing islet cells as they differentiate from their precursors. Upregulated PAI-1 production and decreased gelatinolytic activity correlated to this migration defect. An intact EGF-R pathway appears to be a prerequisite for normal pancreatic development.
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Sand, J., and I. Nordback. "The Differentiation between Pancreatic Neoplastic Cysts and Pancreatic Pseudocyst." Scandinavian Journal of Surgery 94, no. 2 (June 2005): 161–64. http://dx.doi.org/10.1177/145749690509400213.

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The number of small and often asymptomatic cystic lesions detected in pancreas has increased during the last decade. Historically the vast majority of the pancreatic cystic lesions were considered pseudocysts, but in recent series the incidence of various neoplastic cysts, such as intraductal papillary mucinous neoplasm, serous cystadenomas and cystic endocrine tumours, has increased. The possible malignant potential in these cystic neoplasms warrants careful diagnostic workup to choose the optimal treatment for each patient. Patient's age, symptoms and a possible history of acute or chronic pancreatitis with known aetiology together with high quality imaging studies are important in the differential diagnosis between pseudocysts and neoplastic cysts. Endoscopic ultrasound, cyst fluid analysis and positron emission tomography may be used in selected patients, but the accuracy of these methods needs further investigation.
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Kaitsuka, Taku, Kohei Kobayashi, Wakako Otsuka, Takuya Kubo, Farzana Hakim, Fan-Yan Wei, Nobuaki Shiraki, Shoen Kume, and Kazuhito Tomizawa. "Erythropoietin facilitates definitive endodermal differentiation of mouse embryonic stem cells via activation of ERK signaling." American Journal of Physiology-Cell Physiology 312, no. 5 (May 1, 2017): C573—C582. http://dx.doi.org/10.1152/ajpcell.00071.2016.

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Artificially generated pancreatic β-cells from pluripotent stem cells are expected for cell replacement therapy for type 1 diabetes. Several strategies are adopted to direct pluripotent stem cells toward pancreatic differentiation. However, a standard differentiation method for clinical application has not been established. It is important to develop more effective and safer methods for generating pancreatic β-cells without toxic or mutagenic chemicals. In the present study, we screened several endogenous factors involved in organ development to identify the factor, which induced the efficiency of pancreatic differentiation and found that treatment with erythropoietin (EPO) facilitated the differentiation of mouse embryonic stem cells (ESCs) into definitive endoderm. At an early stage of differentiation, EPO treatment significantly increased Sox17 gene expression, as a marker of the definitive endoderm. Contrary to the canonical function of EPO, it did not affect the levels of phosphorylated JAK2 and STAT5, but stimulated the phosphorylation of ERK1/2 and Akt. The MEK inhibitor U0126 significantly inhibited EPO-induced Sox17 expression. The differentiation of ESCs into definitive endoderm is an important step for the differentiation into pancreatic and other endodermal lineages. This study suggests a possible role of EPO in embryonic endodermal development and a new agent for directing the differentiation into endodermal lineages like pancreatic β-cells.
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Tan, Mengtian, Lai Jiang, Yinglei Li, and Wei Jiang. "Dual Inhibition of BMP and WNT Signals Promotes Pancreatic Differentiation from Human Pluripotent Stem Cells." Stem Cells International 2019 (December 1, 2019): 1–15. http://dx.doi.org/10.1155/2019/5026793.

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Pathological or functional loss of pancreatic beta cells is the cause of diabetes. Understanding how signaling pathways regulate pancreatic lineage and searching for combinations of signal modulators to promote pancreatic differentiation will definitely facilitate the robust generation of functional beta cells for curing hyperglycemia. In this study, we first tested the effect of several potent BMP inhibitors on pancreatic differentiation using human embryonic stem cells. Next, we examined the endodermal lineage bias upon potent BMP inhibitor treatment and further checked the crosstalk between signal pathways governing endodermal lineage determination. Furthermore, we improved current pancreatic differentiation system based on the signaling pathway study. Finally, we used human-induced pluripotent stem cells to validate our finding. We found BMP inhibitors indeed not only blocked hepatic lineage but also impeded intestinal lineage from human definitive endoderm unexpectedly. Signaling pathway analysis indicated potent BMP inhibitor resulted in the decrease of WNT signal activity and inhibition of WNT could contribute to the improved pancreatic differentiation. Herein, we combined the dual inhibition of BMP and WNT signaling and greatly enhanced human pancreatic progenitor differentiation as well as beta cell generation from both embryonic stem cells and induced pluripotent stem cells. Conclusively, our present work identified the crosstalk between the BMP and WNT signal pathways during human endoderm patterning and pancreas specification, and provided an improved in vitro pancreatic directed differentiation protocol from human pluripotent stem cells.
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Apelqvist, Åsa, Hao Li, Lukas Sommer, Paul Beatus, David J. Anderson, Tasuku Honjo, Martin Hrabě de Angelis, Urban Lendahl, and Helena Edlund. "Notch signalling controls pancreatic cell differentiation." Nature 400, no. 6747 (August 1999): 877–81. http://dx.doi.org/10.1038/23716.

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Dissertations / Theses on the topic "Pancreatic differentiation"

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Yuan, Songyang. "Differentiation and transdifferentiation of adult pancreatic cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ30425.pdf.

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Myatt, Emily-Jane. "Differentiation of pancreatic and hepatic cell types." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616573.

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The endoderm gives rise to many different cell types including those that will form the liver and pancreas. How cells differentiate during embryonic development is an important focus for the field of regenerative medicine. Understanding the normal development of liver and pancreatic cell types may allow us to develop strategies for the production of hepatocytes and pancreatic beta-cells for therapeutic purposes. One potential method of producing cells for therapeutic purposes is via transdifferentiation, or, the conversion of one cell type to another. In this thesis we aimed to establish a protocol for the transdifferentiation of liver ductal cells (termed cholangiocytes) to either hepatocyte or pancreatic lineages. We also aimed to investigate the signalling pathways important for normal differentiation of embryonic liver and pancreas. In order to address the potential of a cholangiocyte cell line (biliary epithelial cells or BECs) to transdifferentiate to other cell types, BECs were infected with a combination of candidate transcription factors known as ‘master switch’ genes that have previously been demonstrated to induce transdifferentiation to hepatic or pancreatic lineages. We demonstrated that overexpression of the hepatic transcription factors C/EBPα, C/EBPβ and HNF4 resulted in the up-regulation of the hepatocyte genes Albumin and Gs and de novo expression of Afp. In complementary experiments we also demonstrated that overexpression of the pancreatic transcription factors Pdx1, Ngn3, NeuroD and Pax4 resulted in de novo expression of insulin II in BECs. While these results were encouraging further work is necessary to enhance the maturation status of the nascent cells. We also addressed the role of the Notch signalling pathway in the differentiation of embryonic hepatic and pancreatic cells using ex vivo organ culture models of liver and pancreas development. We treated pancreata with N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S- phenylglycine t-Butyl Ester (DAPT) a gamma-secretase inhibitor. Treatment with DAPT inhibits the Notch signalling pathway. Following treatment with DAPT we observed reduced branching morphogenesis, loss of the acinar cell phenotype (amylase expression) and an enhancement in endocrine differentiation (insulin and glucagon expression). We propose that in the absence of Notch signalling the proendocrine gene Ngn3 is no longer repressed by the Notch target Hes1, allowing endocrine differentiation to take place. Finally we observed that β-cells in pancreata treated with DAPT are functionally more mature in terms of responsiveness to glucose stimulation. Overall these results have important implications for the development of potential therapies in the treatment of liver failure and diabetes.
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Decker, Kimberly Jean. "Gata6 regulates pancreatic branching morphogenesis and endocrine differentiation /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 160-175). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Kimura, Yoshito. "ARID1A Maintains Differentiation of Pancreatic Ductal Cells and Inhibits Development of Pancreatic Ductal Adenocarcinoma in Mice." Kyoto University, 2018. http://hdl.handle.net/2433/235986.

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Blyszczuk, Przemyslaw. "Differentiation of embryonic stem cells into pancreatic insulin-producing cells." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97560032X.

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Murad, Nadia Yousif. "Differentiation of human embryonic stem cells to the pancreatic lineage." Thesis, University of Sheffield, 2008. http://etheses.whiterose.ac.uk/6102/.

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Human embryonic stem (hES) cells have great therapeutic potential for the treatment of degenerative conditions such as Parkinson's disease, cardiac failure and type I diabetes. This potential is based on the ability of hES cells in vitro to self-renew and also differentiate to cells of all three germ layers; ectoderm, mesoderm and endoderm. Type I diabetes is due to an autoimmune disease destroying the insulin-secreting cells of the pancreas (β-cells) that regulate plasma glucose concentration. The pancreas develops from the endoderm lineage. 2. To find a cure for type I diabetes based on the use of hES, it is essential to understand the differentiation process of ES cells into the endodermal, β-cell lineage. The aim of this study was to investigate the generation of insulin-secreting cells using hES cells in vitro and to compare sue with those in the developing pancreas of the foetus.
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Shah, Nadia Nisa. "Human embryonic stem cells : prospects for pancreatic β-cell differentiation." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495052.

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The focus of this thesis was to explore different strategies in trying to generate putative pancreatic β-cells using one of the initial Wisconsin H7 hES cell lines. Prior to this, human pancreas development was assessed during the first trimester of pregnancy in an attempt to determine the spatial and temporal expression of development and mature pancreatic β-cell markers during this period. Spontaneous differentiation of hES cells can be induced by the formation of embryoid bodies (EBs) in suspension culture. EBs began to express markers of pancreatic β-cell development and function at a molecular, protein and functional level upon differentiation over a 3-week period. The constitutive over-expression of the terminal β-cell marker PAX4 enhances this process, whereas karyotypic abnormalities induced in hES cells over prolonged culture can hinder differentiation potential towards pancreatic β-cells. Directed differentiation strategies which mimic mouse pancreas development have led to the elucidation of an in vitro protocol to generate putative definitive endoderm from hES cells through the application of Wnt3a and Activin A in the presence of low serum. Indirect co-culture of this H7 hES cell-derived putative definitive endoderm with mouse islets did not lead to the differentiation of fully functional pancreatic β-cells. The hES cell-derived putative definitive endoderm did however influence the aging mouse islets in a positive manner by allowing the maintenance of insulin secretagogue-induced functional responses which are usually lost in culture. This may prove useful in maintaining viability of human islets during culture to be used for transportation therapies.
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Uroić, Daniela Sonja. "Differentiation of embryonic stem cells towards pancreatic β-like cells." Thesis, University of Aberdeen, 2011. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167694.

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Embryonic stem (ES) cells were used as a model system to understand the signalling events in pancreas development. ES cells were differentiated through known precursor stages towards the tissue of interest in order to recapitulate development in vitro. Thus, protocols directing differentiation of mouse ES cells towards definitive endoderm and pancreatic β-cells were developed. A combination of activin A and bone morphogenic protein 4 resulted in a population of enriched cells expressing genetic markers of definitive endoderm. In vitro differentiation of ES cells into functional pancreatic β-cells has only been partially successful, as it results in cells that are not fully differentiated or functional. This might be due to a lack of cues emanating from surrounding cells present in the developing pancreas. Conditioned media from the mouse MIN6 β-cell line were used on the basis that differentiated β- cells might send out signals affecting the differentiation of the surrounding islet cells. Mouse ES cells were enriched in definitive endoderm and then treated with MIN6 conditioned medium. Gene expression of the β-cell markers Insulin1, Insulin2, and Glucose transporter 2 was significantly increased relative to the untreated control group after 10 days of treatment with conditioned medium. This result was specific for conditioned medium from MIN6 cells as conditioned medium from a kidney-, a neuronal-, and an exocrine pancreatic cell line had no effect. In order to characterise the secreted factor(s) the conditioned medium was subjected to protein precipitation. The pancreatic differentiation factor was present in a protein fraction, suggesting that the factor(s) was proteinaceous. The protein in question was neither proinsulin nor insulin. This knowledge will support the efficient generation of insulin-secreting cells for diabetes therapy.
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Chong, Tsz-yat Ian, and 莊子逸. "Inducing the progressive differentiation of hESCs into pancreatic progenitor cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196433.

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Diabetes is a chronic disorder of the pancreas, where a decline in the insulin-producing β-cell population disrupts metabolic homeostasis. Pancreatic transplantation has shown to be effective in circumventing the problem of β-cell insufficiency. However, availability of donor islets remains an obstacle. Although progressive differentiation of embryonic stem cells (ESCs) to pancreatic β-cells is a solution, current protocols are wrought with inefficiencies. It is obvious that to realize ESC differentiation for therapy many steps need to be optimized, and this study describes improvement of Pdx1+pancreatic progenitor derivation, a critical determinant of pancreatic fate. The compounds melatonin and sPDZD2 have been suggested to act through the Protein Kinase A (PKA) pathway to exert transcriptional effects, and in particular sPDZD2 stimulates the expression of pancreatic genes in INS-1E rat pancreatic cells. This led to the hypothesis that the PKA-targeting characteristics of said molecules could be exploited for pancreatic specification through post-translational activation ofPdx1. hESCs were first induced to form definitive endoderm before treatment with melatonin and sPDZD2. Pdx1 expression induced by these molecules was then compared with levels triggered by known pancreatic progenitor inducer Indolactam V (ILV). A secondary objective of this study was to assess the endoderm induction potential of small molecules in hESCs, which claim to be potentially useful in differentiation. In this research, I show that small molecules are noticeably more challenging to use in the hESC context. Between the TGF-β pathwayactivatorsIDE-1 and 2, the latter is more potent at inducing endoderm formation, though it does not surpass the capabilities of Stauprimide, a molecule originally thought to only serve a priming purpose in mESCs.IDE-2 and Stauprimide consistently perform better than Activin A, the near universal factor for endoderm induction. Possible synergy between IDE-2 and Stauprimide was explored, but their combination appears detrimental to Sox17expression. Subsequent pancreatic differentiation was also inefficient, and my results affirm the immaturity of chemically-induced endoderm by contrasting with mainstream means of endoderm induction; levels of endoderm marker expression between the two methods are millions of folds apart. This work exposes the risks of using small molecules, and they necessitate proper characterization before being adopted for differentiation. Most favorably, both sPDZD2 and melatonin were able to trigger Pdx1 expression in STEMDiffTm derived definitive endoderm; 10 and 30folds respectively, comparable to the known Pdx1 inducer ILV (25 folds). I also reveal concentration-mediated differentiation and proliferative purposes of ILV and sPDZD2, which are highly reminiscent of the signaling mechanisms involved during pancreatic development. Preliminary quantification of Pdx1+ cells suggest that high concentrations of ILV and sPDZD2 favor self-renewal of Pdx1+ progenitors, whilst lower doses elevate Pdx1 expression. Demonstration of Pdx1 at both gene and protein expression levels was encouraging, but it remains uncertain if melatonin and sPDZD2 manipulate PKA signaling to exert Pdx1 promoting effects. My work supports the use of melatonin as a candidate for pancreatic differentiation, and suggests involvement of sPDZD2 in deriving and expanding progenitors during pancreatic organogenesis.
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Biochemistry
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Master of Philosophy
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Gsour, Amna. "Differentiation of human cell line towards a pancreatic endocrine lineage." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/differentiation-of-human-cell-line-towards-a-pancreatic-endocrine-lineage(0c2c21fe-724d-449f-804c-02741c89828c).html.

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Islet transplantations have been successful in restoring glucose homeostasis in patients with diabetes; however, the limited number of donor organs limits the success of this treatment. The lineage reprograming of different cell sources to beta cells potentially provides an unlimited supply of insulin-producing cells for regenerative therapy for patients with diabetes. The aim of this study was to investigate the ability to transdifferentiate two cell lines into an endocrine lineage. Insulin production in pancreatic beta cells can be increased using a small molecule, 3,5-disubstituted isoxazole, N-cyclopropyl-t-(thiophen-2-yl)isoxazole-3-carboxamide (isoxazole) but its effect on other cell types has not been reported. Here, we investigated the lineage reprogramming of PANC-1 pancreatic ductal cells to insulin producing cells by isoxazole treatment. Gene expression was performed using RT-PCR and qPCR for approximately 30 genes critical to beta cell development and function. In addition, quantitative proteomic profiling was performed using LC-MS by monitoring protein abundance in isoxazole-treated PANC-1 cells compared to time-matched controls. Isoxazole treatment stimulated PANC-1 cells to aggregate into islet-like clusters and gene expression analysis revealed induction of important developmental beta cell markers including NGN3, NEUROD1 and INSULIN. In addition, beta cell surface markers were also upregulated such as CD200, GPR50, TROP-2, GLUT2 and SLC30A8. Using LC-MS a catalogue of approximately 2400 identified proteins was generated; 257 proteins were differentially expressed in isoxazole-treated cells compared to DMSO-vehicle controls at p < 0.05. Amongst the proteins upregulated were molecules that regulate metabolic processes and cytoskeletal reorganisation. The expression of the majority of these proteins has not been previously reported or studied in the context of beta cell differentiation. Functional analysis of the relative protein changes was determined using Ingenuity Pathway Analysis, IPA, and gene ontology, GO, software, which revealed the regulation of several cellular canonical pathways including metabolic pathways, cell adhesion, remodelling of epithelial adherens junctions and actin cytoskeleton signalling. The effects of isoxazole were further studied in the A549 lung cancer cell line. Similar effects were observed, such as the induction of pro-endocrine markers NGN3 and NEUROD1 and endocrine-specific hormones INS and GCG. These results indicate that isoxazole has the capacity to transdifferentiate pancreatic and non-pancreatic cell origins into an endocrine lineage. This study reveals the powerful induction capacity of isoxazole in inducing cellular reprogramming events.
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Books on the topic "Pancreatic differentiation"

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service), SpringerLink (Online, ed. Pancreatic Stem Cells. Totowa, NJ: Humana Press, 2009.

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Book chapters on the topic "Pancreatic differentiation"

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Fishman, Bettina, Hanna Segev, and Joseph Itskovitz-Eldor. "Pancreatic Cell Differentiation." In Human Cell Culture, 189–209. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-5983-4_11.

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Domínguez-Bendala, Juan. "Stem Cell Differentiation: General Approaches." In Pancreatic Stem Cells, 51–61. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-132-5_4.

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Domínguez-Bendala, Juan. "Embryonic Stem Cells and Pancreatic Differentiation." In Pancreatic Stem Cells, 63–80. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-132-5_5.

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Domínguez-Bendala, Juan. "Adult Stem Cells and Pancreatic Differentiation." In Pancreatic Stem Cells, 81–89. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-132-5_6.

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Lumelsky, Nadya. "Pancreatic Differentiation of Pluripotent Stem Cells." In Human Embryonic Stem Cells, 161–79. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-423-8_9.

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Curley, P., and M. J. McMahon. "Is Differentiation of Haemorrhagic from Oedematous Acute Pancreatitis of Clinical Importance?" In Standards in Pancreatic Surgery, 99–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77437-9_11.

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Vinckier, Nicholas, Jinzhao Wang, and Maike Sander. "Pancreatic Differentiation from Human Pluripotent Stem Cells." In Working with Stem Cells, 257–75. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30582-0_15.

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Sakano, Daisuke, Nobuaki Shiraki, and Shoen Kume. "Pancreatic Differentiation from Murine Embryonic Stem Cells." In Embryonic Stem Cell Protocols, 417–23. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/7651_2015_217.

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Yoon, Hong Jin, Sung Ill Jang, and Dong Ki Lee. "Differentiation of Indeterminate Biliary Stricture." In Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases, 127–41. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-0608-2_9.

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Schroeder, Insa S., Anna Daniel-Wojcik, and Anna M. Wobus. "Strategies for Pancreatic Differentiation of Pluripotent Stem Cells." In Proceedings of the 21st Annual Meeting of the European Society for Animal Cell Technology (ESACT), Dublin, Ireland, June 7-10, 2009, 177–87. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0884-6_28.

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Conference papers on the topic "Pancreatic differentiation"

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Breunig, M., M. Hohwieler, T. Seufferlein, S. Liebau, and A. Kleger. "PPDPF impacts pancreatic differentiation of human pluripotent stem cell derived pancreatic organoids." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604922.

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Khamaysi, I., A. Abu Ammar, G. Vasilyev, A. Arenstein, Y. Chowers, and E. Zussman. "DIFFERENTIATION OF PANCREATIC CYST TYPES BY ANALYSIS OF RHEOLOGICAL BEHAVIOR OF PANCREATIC CYST FLUID." In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681298.

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Patricia Olar, M., O. Mosteanu, I. Rusu, and A. Seicean. "DIFFERENTIATION OF PANCREATIC CYSTS BY CONTRAST-ENHANCED ENDOSCOPIC ULTRASONOGRAPHY." In ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637205.

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Peverley, Louise V., Christopher J. Halbrook, Jason C. Hall, Christine M. Ardito, and Howard C. Crawford. "Abstract A77: Investigating the role of ADAM10 in pancreatic tumor differentiation." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a77.

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Zhang, Yaqing, Katelyn L. Donahue, Wei Yan, Zeribe C. Nwosu, Kristee L. Brown, Sion Yang, Howard C. Crawford, et al. "Abstract PO-063: Regulatory T cells regulate fibroblast differentiation during pancreatic carcinogenesis." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-po-063.

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Shi, Kerong, Vaishali Parekh, Swarnava Roy, and Sunita K. Agarwal. "Abstract LB-140: Menin-mediated regulation of pancreatic β-cell differentiation factors." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-140.

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Placencio-Hickok, Veronica R., Arsen Osipov, Sejal Mehta, Subhash D. Katewa, Jiping Zha, and Andrew E. Hendifar. "Abstract PO-001: Increased growth differentiation factor 15 serum levels in pancreatic cancer patients." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-po-001.

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Alanio, Cecile, Bertram Bengsch, Josephine R. Gies, Sarah Henrickson, Nan Ping Weng, Janáe A. Ritz-Romeo, Mark O'Hara, et al. "Abstract A123: Skewed CD4 and CD8 T-cell differentiation in pancreatic cancer patients." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a123.

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Gong, Jun, Raymond Gong, Richard T. Waldron, Aurelia Lugea, and Stephen J. Pandol. "Abstract 5353: Leptin regulates cell differentiation and protumorigenic responses in pancreatic stellate cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5353.

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Krah, Nathan M., Deanne E. Yugawa, Julie A. Straley, Shuba M. Narayanan, Ana C. Azevedo-Pouly, and L. Charles Murtaugh. "Abstract B06: Maintenance of acinar cell differentiation prevents KRAS-driven pancreatic cancer initiation." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b06.

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