Статті в журналах: "Pancreas Organogenesis"

1

Hammerman, Marc R. "Organogenesis of the endocrine pancreas." Kidney International 68, no. 5 (November 2005): 1953–55. http://dx.doi.org/10.1111/j.1523-1755.2005.00628.x.

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2

Grapin-Botton, A. "Three-dimensional pancreas organogenesis models." Diabetes, Obesity and Metabolism 18 (September 2016): 33–40. http://dx.doi.org/10.1111/dom.12720.

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3

McLin, Valerie A., and Aaron M. Zorn. "Organogenesis: Making Pancreas from Liver." Current Biology 13, no. 3 (February 2003): R96—R98. http://dx.doi.org/10.1016/s0960-9822(03)00036-8.

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4

Gnatenko, D. A., E. P. Kopantzev, and E. D. Sverdlov. "Fibroblast growth factors and their effects in pancreas organogenesis." Biomeditsinskaya Khimiya 63, no. 3 (2017): 211–18. http://dx.doi.org/10.18097/pbmc20176303211.

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Fibroblast growth factors (FGF) – growth factors that regulate many important biological processes, including proliferation and differentiation of embryonic cells during organogenesis. In this review, we will summarize current information about the involvement of FGFs in the pancreas organogenesis. Pancreas organogenesis is a complex process, which involves constant signaling from mesenchymal tissue. This orchestrates the activation of various regulator genes at specific stages, determining the specification of progenitor cells. Alterations in FGF/FGFR signaling pathway during this process lead to incorrect activation of the master genes, which leads to different pathologies during pancreas development. Understanding the full picture about role of FGF factors in pancreas development will make it possible to more accurately understand their role in other pathologies of this organ, including carcinogenesis.

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5

Hammerman, Marc R. "Organogenesis of Kidney and Endocrine Pancreas." Organogenesis 3, no. 2 (October 2007): 59–66. http://dx.doi.org/10.4161/org.3.2.5382.

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6

Gnatenko, D. A., E. P. Kopantsev, and E. D. Sverdlov. "Fibroblast growth factors and pancreas organogenesis." Biochemistry (Moscow), Supplement Series B: Biomedical Chemistry 11, no. 4 (October 2017): 341–48. http://dx.doi.org/10.1134/s1990750817040023.

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7

Cano, David A., Bernat Soria, Francisco Martín, and Anabel Rojas. "Transcriptional control of mammalian pancreas organogenesis." Cellular and Molecular Life Sciences 71, no. 13 (November 13, 2013): 2383–402. http://dx.doi.org/10.1007/s00018-013-1510-2.

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8

Kim, Seung K., Matthias Hebrok, En Li, S. Paul Oh, Heinrich Schrewe, Erin B. Harmon, Joon S. Lee, and Douglas A. Melton. "Activin receptor patterning of foregut organogenesis." Genes & Development 14, no. 15 (August 1, 2000): 1866–71. http://dx.doi.org/10.1101/gad.14.15.1866.

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Foregut development produces a characteristic sequence of gastrointestinal and respiratory organs, but the signaling pathways that ensure this developmental order remain largely unknown. Here, mutations of activin receptors ActRIIA and ActRIIB are shown to disrupt the development of posterior foregut-derived organs, including the stomach, pancreas, and spleen. Foregut expression of genes includingShh and Isl1 is shifted in mutant mice. The endocrine pancreas is particularly sensitive to the type and extent of receptor inactivation. ActRIIA+/−B+/−animals lack axial defects, but have hypoplastic pancreatic islets, hypoinsulinemia, and impaired glucose tolerance. Thus, activin receptor-mediated signaling regulates axial patterning, cell differentiation, and function of foregut-derived organs.

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9

Carrasco, Manuel, Irene Delgado, Bernat Soria, Francisco Martín, and Anabel Rojas. "GATA4 and GATA6 control mouse pancreas organogenesis." Journal of Clinical Investigation 122, no. 10 (October 1, 2012): 3504–15. http://dx.doi.org/10.1172/jci63240.

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10

Shih, Hung Ping, Allen Wang, and Maike Sander. "Pancreas Organogenesis: From Lineage Determination to Morphogenesis." Annual Review of Cell and Developmental Biology 29, no. 1 (October 6, 2013): 81–105. http://dx.doi.org/10.1146/annurev-cellbio-101512-122405.

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11

Louw, Johan, and Sonia Wolfe-Coote. "Introduction to endocrine pancreas organogenesis and neogenesis." Microscopy Research and Technique 43, no. 4 (November 15, 1998): 283. http://dx.doi.org/10.1002/(sici)1097-0029(19981115)43:4<283::aid-jemt1>3.0.co;2-4.

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12

Hammerman, Marc R. "Organogenesis of endocrine pancreas from transplanted embryonic anlagen." Transplant Immunology 12, no. 3-4 (April 2004): 249–58. http://dx.doi.org/10.1016/j.trim.2003.12.003.

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13

Larsen, Hjalte List, and Anne Grapin-Botton. "The molecular and morphogenetic basis of pancreas organogenesis." Seminars in Cell & Developmental Biology 66 (June 2017): 51–68. http://dx.doi.org/10.1016/j.semcdb.2017.01.005.

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14

Bramswig, Nuria C., and Klaus H. Kaestner. "Organogenesis and functional genomics of the endocrine pancreas." Cellular and Molecular Life Sciences 69, no. 13 (January 13, 2012): 2109–23. http://dx.doi.org/10.1007/s00018-011-0915-z.

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15

Talavera-Adame, Dodanim. "Endothelium-derived essential signals involved in pancreas organogenesis." World Journal of Experimental Medicine 5, no. 2 (2015): 40. http://dx.doi.org/10.5493/wjem.v5.i2.40.

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16

&NA;. "ORGANOGENESIS OF THE EMBRYONIC PANCREAS ALLOGRAFTED INTO RATS." Transplantation 82, Suppl 2 (July 2006): 863. http://dx.doi.org/10.1097/00007890-200607152-02407.

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17

Pan, Fong Cheng, and Chris Wright. "Pancreas organogenesis: From bud to plexus to gland." Developmental Dynamics 240, no. 3 (February 17, 2011): 530–65. http://dx.doi.org/10.1002/dvdy.22584.

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18

Minami, Kohtaro. "GATA transcription factors: New key regulators in pancreas organogenesis." Journal of Diabetes Investigation 4, no. 5 (May 12, 2013): 426–27. http://dx.doi.org/10.1111/jdi.12089.

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19

Scheibner, Katharina, Mostafa Bakhti, Aimée Bastidas-Ponce, and Heiko Lickert. "Wnt signaling: implications in endoderm development and pancreas organogenesis." Current Opinion in Cell Biology 61 (December 2019): 48–55. http://dx.doi.org/10.1016/j.ceb.2019.07.002.

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20

Sakakura, T., I. Kusano, M. Kusakabe, Y. Inaguma, and Y. Nishizuka. "Biology of mammary fat pad in fetal mouse: capacity to support development of various fetal epithelia in vivo." Development 100, no. 3 (July 1, 1987): 421–30. http://dx.doi.org/10.1242/dev.100.3.421.

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Epithelia from the lobular part of submandibular salivary gland, glandular stomach, intestine and colon of 14-day C3H/HeN fetuses, and from pituitary gland and pancreas of 12-day fetuses were recombined with 14-day mammary fat pad precursor tissue and syngrafted under the kidney capsule. The normal organogenetic development typical of the epithelium occurred. The same epithelia taken from earlier stage fetuses did not develop normally. Thus, 14-day fetal mouse mammary fat pad precursor tissue has the capacity to support normal organogenesis of various fetal epithelia of developmentally advanced stages. This supportive capacity is decreased in the fat pad precursor tissue of 17- to 18-day fetal mice and is entirely lost postnatally.

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21

Crane, Andrew T., Rajagopal N. Aravalli, Atsushi Asakura, Andrew W. Grande, Venkatramana D. Krishna, Daniel F. Carlson, Maxim C. J. Cheeran, et al. "Interspecies Organogenesis for Human Transplantation." Cell Transplantation 28, no. 9-10 (August 19, 2019): 1091–105. http://dx.doi.org/10.1177/0963689719845351.

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Blastocyst complementation combined with gene editing is an emerging approach in the field of regenerative medicine that could potentially solve the worldwide problem of organ shortages for transplantation. In theory, blastocyst complementation can generate fully functional human organs or tissues, grown within genetically engineered livestock animals. Targeted deletion of a specific gene(s) using gene editing to cause deficiencies in organ development can open a niche for human stem cells to occupy, thus generating human tissues. Within this review, we will focus on the pancreas, liver, heart, kidney, lung, and skeletal muscle, as well as cells of the immune and nervous systems. Within each of these organ systems, we identify and discuss (i) the common causes of organ failure; (ii) the current state of regenerative therapies; and (iii) the candidate genes to knockout and enable specific exogenous organ development via the use of blastocyst complementation. We also highlight some of the current barriers limiting the success of blastocyst complementation.

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22

Dettmer, Rabea, Karsten Cirksena, Julia Münchhoff, Jasmin Kresse, Ulf Diekmann, Isabell Niwolik, Falk F. R. Buettner, and Ortwin Naujok. "FGF2 Inhibits Early Pancreatic Lineage Specification during Differentiation of Human Embryonic Stem Cells." Cells 9, no. 9 (August 20, 2020): 1927. http://dx.doi.org/10.3390/cells9091927.

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Growth factors are important regulators during organ development. For many vertebrates (but not humans) it is known how they contribute to the formation and expansion of PDX1-positive cells during pancreas organogenesis. Here, the effects of the fibroblast growth factors FGF2, FGF7, FGF10, and epidermal growth factor (EGF) on pancreas development in humans were assessed by using human pluripotent stem cells (hPSCs). During this, FGF2 was identified as a potent anti-pancreatic factor whereas FGF7, FGF10, and EGF increased the cell mass while retaining PDX1-positivity. FGF2 increased the expression of the anti-pancreatic factor sonic hedgehog (SHH) while suppressing PDX1 in a dose-dependent manner. Differentiating cells secreted SHH to the medium and we interrogated the cells’ secretome during differentiation to globally examine the composition of secreted signaling factors. Members of the TGF-beta-, Wnt-, and FGF-pathways were detected. FGF17 showed a suppressive anti-pancreatic effect comparable to FGF2. By inhibition of specific branches of FGF-receptor signaling, we allocated the SHH-induction by FGF2 to MEK/ERK-signaling and the anti-pancreatic effect of FGF2 to the receptor variant FGFR1c or 3c. Altogether, we report findings on the paracrine activity of differentiating hPSCs during generation of pancreatic progenitors. These observations suggest a different role for FGF2 in humans compared to animal models of pancreas organogenesis.

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23

Rovira, Meritxell, Goutham Atla, Miguel Angel Maestro, Vane Grau, Javier García-Hurtado, Maria Maqueda, Jose Luis Mosquera, et al. "REST is a major negative regulator of endocrine differentiation during pancreas organogenesis." Genes & Development 35, no. 17-18 (August 12, 2021): 1229–42. http://dx.doi.org/10.1101/gad.348501.121.

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Multiple transcription factors have been shown to promote pancreatic β-cell differentiation, yet much less is known about negative regulators. Earlier epigenomic studies suggested that the transcriptional repressor REST could be a suppressor of endocrinogenesis in the embryonic pancreas. However, pancreatic Rest knockout mice failed to show abnormal numbers of endocrine cells, suggesting that REST is not a major regulator of endocrine differentiation. Using a different conditional allele that enables profound REST inactivation, we observed a marked increase in pancreatic endocrine cell formation. REST inhibition also promoted endocrinogenesis in zebrafish and mouse early postnatal ducts and induced β-cell-specific genes in human adult duct-derived organoids. We also defined genomic sites that are bound and repressed by REST in the embryonic pancreas. Our findings show that REST-dependent inhibition ensures a balanced production of endocrine cells from embryonic pancreatic progenitors.

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24

Sakhneny, Lina, Laura Khalifa-Malka, and Limor Landsman. "Pancreas organogenesis: Approaches to elucidate the role of epithelial-mesenchymal interactions." Seminars in Cell & Developmental Biology 92 (August 2019): 89–96. http://dx.doi.org/10.1016/j.semcdb.2018.08.012.

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25

Azizoglu, D. Berfin, and Ondine Cleaver. "Blood vessel crosstalk during organogenesis-focus on pancreas and endothelial cells." Wiley Interdisciplinary Reviews: Developmental Biology 5, no. 5 (June 21, 2016): 598–617. http://dx.doi.org/10.1002/wdev.240.

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26

Hebrok, M., S. K. Kim, B. St Jacques, A. P. McMahon, and D. A. Melton. "Regulation of pancreas development by hedgehog signaling." Development 127, no. 22 (November 15, 2000): 4905–13. http://dx.doi.org/10.1242/dev.127.22.4905.

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Pancreas organogenesis is regulated by the interaction of distinct signaling pathways that promote or restrict morphogenesis and cell differentiation. Previous work has shown that activin, a TGF(beta+) signaling molecule, permits pancreas development by repressing expression of Sonic hedgehog (Shh), a member of the hedgehog family of signaling molecules that antagonize pancreas development. Here we show that Indian hedgehog (Ihh), another hedgehog family member, and Patched 1 (Ptc1), a receptor and negative regulator of hedgehog activity, are expressed in pancreatic tissue. Targeted inactivation of Ihh in mice allows ectopic branching of ventral pancreatic tissue resulting in an annulus that encircles the duodenum, a phenotype frequently observed in humans suffering from a rare disorder known as annular pancreas. Shh(−)(/)(−) and Shh(−)(/)(−) Ihh(+/)(−) mutants have a threefold increase in pancreas mass, and a fourfold increase in pancreatic endocrine cell numbers. In contrast, mutations in Ptc1 reduce pancreas gene expression and impair glucose homeostasis. Thus, islet cell, pancreatic mass and pancreatic morphogenesis are regulated by hedgehog signaling molecules expressed within and adjacent to the embryonic pancreas. Defects in hedgehog signaling may lead to congenital pancreatic malformations and glucose intolerance.

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27

Rouet-Karama, Solange, and Jacques Albert. "Organogenesis and differentiation of the pancreas in the toad Bufo bufo L." Roux's Archives of Developmental Biology 197, no. 3 (May 1988): 148–56. http://dx.doi.org/10.1007/bf00427918.

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28

Sjödin, Anders, Ulf Dahl, and Henrik Semb. "Mouse R-Cadherin: Expression during the Organogenesis of Pancreas and Gastrointestinal Tract." Experimental Cell Research 221, no. 2 (December 1995): 413–25. http://dx.doi.org/10.1006/excr.1995.1392.

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29

Jeng, Kuo-Shyang, Chiung-Fang Chang, and Shu-Sheng Lin. "Sonic Hedgehog Signaling in Organogenesis, Tumors, and Tumor Microenvironments." International Journal of Molecular Sciences 21, no. 3 (January 23, 2020): 758. http://dx.doi.org/10.3390/ijms21030758.

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During mammalian embryonic development, primary cilia transduce and regulate several signaling pathways. Among the various pathways, Sonic hedgehog (SHH) is one of the most significant. SHH signaling remains quiescent in adult mammalian tissues. However, in multiple adult tissues, it becomes active during differentiation, proliferation, and maintenance. Moreover, aberrant activation of SHH signaling occurs in cancers of the skin, brain, liver, gallbladder, pancreas, stomach, colon, breast, lung, prostate, and hematological malignancies. Recent studies have shown that the tumor microenvironment or stroma could affect tumor development and metastasis. One hypothesis has been proposed, claiming that the pancreatic epithelia secretes SHH that is essential in establishing and regulating the pancreatic tumor microenvironment in promoting cancer progression. The SHH signaling pathway is also activated in the cancer stem cells (CSC) of several neoplasms. The self-renewal of CSC is regulated by the SHH/Smoothened receptor (SMO)/Glioma-associated oncogene homolog I (GLI) signaling pathway. Combined use of SHH signaling inhibitors and chemotherapy/radiation therapy/immunotherapy is therefore key in targeting CSCs.

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30

De Angelis, Maria Teresa, Filomena Russo, Fulvio D’Angelo, Antonella Federico, Marica Gemei, Luigi Del Vecchio, Michele Ceccarelli, Mario De Felice, and Geppino Falco. "Novel Pancreas Organogenesis Markers Refine the Pancreatic Differentiation Roadmap of Embryonic Stem cells." Stem Cell Reviews and Reports 10, no. 2 (January 5, 2014): 269–79. http://dx.doi.org/10.1007/s12015-013-9489-5.

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31

Briffa, Jessica F., Andrew J. McAinch, Tania Romano, Mary E. Wlodek, and Deanne H. Hryciw. "Leptin in pregnancy and development: a contributor to adulthood disease?" American Journal of Physiology-Endocrinology and Metabolism 308, no. 5 (March 1, 2015): E335—E350. http://dx.doi.org/10.1152/ajpendo.00312.2014.

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Emerging research has highlighted the importance of leptin in fetal growth and development independent of its essential role in the maintenance of hunger and satiety through the modulation of neuropeptide Y and proopiomelanocortin neurons. Alterations in maternal-placental-fetal leptin exchange may modify the development of the fetus and contribute to the increased risk of developing disease in adulthood. In addition, leptin also plays an important role in reproductive functions, with plasma leptin concentrations rising in pregnant women, peaking during the third trimester. Elevated plasma leptin concentrations occur at the completion of organogenesis, and research in animal models has demonstrated that leptin is involved in the development and maturation of a number of organs, including the heart, brain, kidneys, and pancreas. Elevated maternal plasma leptin is associated with maternal obesity, and reduced fetal plasma leptin is correlated with intrauterine growth restriction. Alterations in plasma leptin during development may be associated with an increased risk of developing a number of adulthood diseases, including cardiovascular, metabolic, and renal diseases via altered fetal development and organogenesis. Importantly, research has shown that leptin antagonism after birth significantly reduces maturation of numerous organs. Conversely, restoration of the leptin deficiency after birth in growth-restricted animals restores the offspring's body weight and improves organogenesis. Therefore, leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood. Therefore, greater understanding of the role of leptin during development may assist in the prevention and treatment of a number of disease states that occur in adulthood.

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32

Bhushan, Anil, Nobuyuki Itoh, Shigeaki Kato, Jean P. Thiery, Paul Czernichow, Saverio Bellusci, and Raphael Scharfmann. "Fgf10 is essential for maintaining the proliferative capacity of epithelial progenitor cells during early pancreatic organogenesis." Development 128, no. 24 (December 15, 2001): 5109–17. http://dx.doi.org/10.1242/dev.128.24.5109.

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The importance of mesenchymal-epithelial interactions for the proper development of the pancreas has been acknowledged since the early 1960s, even though the molecule(s) mediating this process have remained unknown. We demonstrate here that Fgf10, a member of the fibroblast growth factor family (FGFs), plays an essential role in this process. We show that Fgf10 is expressed in the mesenchyme directly adjacent to the early dorsal and ventral pancreatic epithelial buds. In Fgf10–/– mouse embryos, the evagination of the epithelium and the initial formation of the dorsal and ventral buds appear normal. However, the subsequent growth, differentiation and branching morphogenesis of the pancreatic epithelium are arrested; this is primarily due to a dramatic reduction in the proliferation of the epithelial progenitor cells marked by the production of the homeobox protein PDX1. Furthermore, FGF10 restores the population of PDX1-positive cells in organ cultures derived from Fgf10–/– embryos. These results indicate that Fgf10 signalling is required for the normal development of the pancreas and should prove useful in devising methods to expand pancreatic progenitor cells.

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33

Kim, Junchul, Sang-Woo Lee, and Kyungpyo Park. "CXCR4 Regulates Temporal Differentiation via PRC1 Complex in Organogenesis of Epithelial Glands." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 619. http://dx.doi.org/10.3390/ijms22020619.

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CXC-chemokine receptor type 4 (CXCR4), a 7-transmembrane receptor family member, displays multifaceted roles, participating in immune cell migration, angiogenesis, and even adipocyte metabolism. However, the activity of such a ubiquitously expressed receptor in epithelial gland organogenesis has not yet been fully explored. To investigate the relationship between CXCL12/CXCR4 signaling and embryonic glandular organogenesis, we used an ex vivo culture system with live imaging and RNA sequencing to elucidate the transcriptome and protein-level signatures of AMD3100, a potent abrogating reagent of the CXCR4-CXCL12 axis, imprinted on the developing organs. Immunostaining results showed that CXCR4 was highly expressed in embryonic submandibular gland, lung, and pancreas, especially at the periphery of end buds containing numerous embryonic stem/progenitor cells. Despite no significant increase in apoptosis, AMD3100-treated epithelial organs showed a retarded growth with significantly slower branching and expansion. Further analyses with submandibular glands revealed that such responses resulted from the AMD3100-induced precocious differentiation of embryonic epithelial cells, losing mitotic activity. RNA sequencing analysis revealed that inhibition of CXCR4 significantly down-regulated polycomb repressive complex (PRC) components, known as regulators of DNA methylation. Treatment with PRC inhibitor recapitulated the AMD3100-induced precocious differentiation. Our results indicate that the epigenetic modulation by the PRC-CXCR12/CXCR4 signaling axis is crucial for the spatiotemporal regulation of proliferation and differentiation of embryonic epithelial cells during embryonic glandular organogenesis.

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34

Kim, Junchul, Sang-Woo Lee, and Kyungpyo Park. "CXCR4 Regulates Temporal Differentiation via PRC1 Complex in Organogenesis of Epithelial Glands." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 619. http://dx.doi.org/10.3390/ijms22020619.

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Анотація:

CXC-chemokine receptor type 4 (CXCR4), a 7-transmembrane receptor family member, displays multifaceted roles, participating in immune cell migration, angiogenesis, and even adipocyte metabolism. However, the activity of such a ubiquitously expressed receptor in epithelial gland organogenesis has not yet been fully explored. To investigate the relationship between CXCL12/CXCR4 signaling and embryonic glandular organogenesis, we used an ex vivo culture system with live imaging and RNA sequencing to elucidate the transcriptome and protein-level signatures of AMD3100, a potent abrogating reagent of the CXCR4-CXCL12 axis, imprinted on the developing organs. Immunostaining results showed that CXCR4 was highly expressed in embryonic submandibular gland, lung, and pancreas, especially at the periphery of end buds containing numerous embryonic stem/progenitor cells. Despite no significant increase in apoptosis, AMD3100-treated epithelial organs showed a retarded growth with significantly slower branching and expansion. Further analyses with submandibular glands revealed that such responses resulted from the AMD3100-induced precocious differentiation of embryonic epithelial cells, losing mitotic activity. RNA sequencing analysis revealed that inhibition of CXCR4 significantly down-regulated polycomb repressive complex (PRC) components, known as regulators of DNA methylation. Treatment with PRC inhibitor recapitulated the AMD3100-induced precocious differentiation. Our results indicate that the epigenetic modulation by the PRC-CXCR12/CXCR4 signaling axis is crucial for the spatiotemporal regulation of proliferation and differentiation of embryonic epithelial cells during embryonic glandular organogenesis.

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35

Moriya, Naomi, Shinji Komazaki, and Makoto Asashima. "In vitro organogenesis of pancreas in Xenopus laevis dorsal lips treated with retinoic acid." Development, Growth and Differentiation 42, no. 2 (April 9, 2000): 175–85. http://dx.doi.org/10.1046/j.1440-169x.2000.00498.x.

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36

Bort, R. "Hex homeobox gene-dependent tissue positioning is required for organogenesis of the ventral pancreas." Development 131, no. 4 (January 21, 2004): 797–806. http://dx.doi.org/10.1242/dev.00965.

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37

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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Анотація:

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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38

Feurle, Gerhard E., Gerd Hamscher, and Ali E. Firat. "The Role of CCK and Its Analogues in the Organogenesis of the Fetal Rat Pancreas." Pancreas 10, no. 3 (April 1995): 281–86. http://dx.doi.org/10.1097/00006676-199504000-00010.

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39

Arregi, Igor, Maria Climent, Dobromir Iliev, Jürgen Strasser, Nadège Gouignard, Jenny K. Johansson, Tania Singh, et al. "Retinol Dehydrogenase-10 Regulates Pancreas Organogenesis and Endocrine Cell Differentiation via Paracrine Retinoic Acid Signaling." Endocrinology 157, no. 12 (October 14, 2016): 4615–31. http://dx.doi.org/10.1210/en.2016-1745.

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40

Kamaci, H. Okan, Cüneyt Suzer, Deniz Çoban, Şahin Saka, and Kürşat Firat. "Organogenesis of exocrine pancreas in sharpsnout sea bream (Diplodus puntazzo) larvae: characterization of trypsin expression." Fish Physiology and Biochemistry 36, no. 4 (January 14, 2010): 993–1000. http://dx.doi.org/10.1007/s10695-009-9377-8.

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41

Lo, Bryan, Geraldine Strasser, Meredith Sagolla, Cary D. Austin, Melissa Junttila, and Ira Mellman. "Lkb1 regulates organogenesis and early oncogenesis along AMPK-dependent and -independent pathways." Journal of Cell Biology 199, no. 7 (December 24, 2012): 1117–30. http://dx.doi.org/10.1083/jcb.201208080.

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The tumor suppressor Lkb1/STK11/Par-4 is a key regulator of cellular energy, proliferation, and polarity, yet its mechanisms of action remain poorly defined. We generated mice harboring a mutant Lkb1 knockin allele that allows for rapid inhibition of Lkb1 kinase. Culturing embryonic tissues, we show that acute loss of kinase activity perturbs epithelial morphogenesis without affecting cell polarity. In pancreas, cystic structures developed rapidly after Lkb1 inhibition. In lung, inhibition resulted in cell-autonomous branching defects. Although the lung phenotype was rescued by an activator of the Lkb1 target adenosine monophosphate–activated kinase (AMPK), pancreatic cyst development was independent of AMPK signaling. Remarkably, the pancreatic phenotype evolved to resemble precancerous lesions, demonstrating that loss of Lkb1 was sufficient to drive the initial steps of carcinogenesis ex vivo. A similar phenotype was induced by expression of mutant K-Ras with p16/p19 deletion. Combining culture of embryonic tissues with genetic manipulation and chemical genetics thus provides a powerful approach to unraveling developmental programs and understanding cancer initiation.

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42

Kayed, H., J. Kleeff, S. Keleg, MW Buchler, and H. Friess. "Distribution of Indian hedgehog and its receptors patched and smoothened in human chronic pancreatitis." Journal of Endocrinology 178, no. 3 (September 1, 2003): 467–78. http://dx.doi.org/10.1677/joe.0.1780467.

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Indian hedgehog (IHH) and its receptors patched (PTC) and smoothened (SMO) belong to the hedgehog family of signaling molecules, which are essential for a variety of patterning events during mammalian tIssue development. IHH plays a role in pancreas organogenesis and differentiation, as well as in the regulation of insulin production. In the present study, the expression of IHH and its receptors was analyzed in normal human pancreatic and chronic pancreatitis (CP) tIssues using Northern blotting, immunohistochemistry and Western blotting, and was correlated with clinicopathological parameters. In addition, the effects of inhibition and stimulation of the hedgehog signaling pathway on cell growth were determined in TAKA-1 normal pancreatic ductal cells. IHH mRNA was expressed in the normal human pancreas and CP tIssues, with slightly higher expression levels in CP. Using immunohistochemistry, IHH and its receptors were localized mainly in the islet cells of the normal pancreas. In CP, IHH and its receptors were present in the cells forming tubular complexes and in the islets with a different signal pattern compared with the islets in the normal pancreas. Correlation between diabetic and non-diabetic CP patients revealed no significant difference in IHH, SMO, or PTC immunoreactivity. Inhibition of hedgehog signaling in TAKA-1 pancreatic ductal cells using cyclopamine significantly reduced their growth through cell cycle arrest, while stimulation of the IHH pathway enhanced the growth of these cells. In conclusion, IHH and its receptors are expressed in the normal human pancreas and in CP, yet with a different distribution and cellular localization. IHH signaling may be involved in the pathogenesis of CP, i.e. in the formation and proliferation of tubular complexes and in islet cell dysfunction.

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43

Hammerman, Marc R. "Xenotransplantation of Embryonic Pig Kidney or Pancreas to Replace the Function of Mature Organs." Journal of Transplantation 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/501749.

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Lack of donor availability limits the number of human donor organs. The need for host immunosuppression complicates transplantation procedures. Ultrastructurally precise kidneys differentiate in situ following xenotransplantation in mesentery of embryonic pig renal primordia. The developing organ attracts its blood supply from the host, obviating humoral rejection. Engraftment of pig renal primordia transplanted directly into rats requires host immune suppression. However, insulin-producing cells originating from embryonic pig pancreas obtained very early following initiation of organogenesis [embryonic day 28 (E28)] engraft long term in nonimmune-suppressed diabetic rats or rhesus macaques. Engraftment of morphologically similar cells originating from adult porcine islets of Langerhans (islets) occurs in rats previously transplanted with E28 pig pancreatic primordia. Here, we review recent findings germane to xenotransplantation of pig renal or pancreatic primordia as a novel organ replacement strategy.

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44

de Pablo, F., R. Dashner, A. R. Shuldiner, and J. Roth. "Xenopus laevis oocytes, eggs and tadpoles contain immunoactive insulin." Journal of Endocrinology 141, no. 1 (April 1994): 123–29. http://dx.doi.org/10.1677/joe.0.1410123.

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Abstract Insulin is a multifunctional polypeptide hormone that regulates metabolic processes and promotes mitogenesis and differentiation in vitro in the cells and tissues of several species. Its role in vivo during embryogenesis is still poorly understood. We have previously found insulin mRNA in mature Xenopus laevis oocytes and in embryos during neurulation (before organogenesis of the pancreas takes place). We have now measured insulin immunoactivity in mature oocytes, unfertilized eggs and day-2 tadpoles. Using reversed phase high performance liquid chromatography, we found low levels of insulin in extracts of oocytes (stage VI). Both Xenopus insulin I and II were detected in unfertilized eggs. The day-2 tadpoles (stages 31–33) also contained immunoactive insulin, and in swimming tadpoles (stage 46) a few clusters of cells containing insulin immunoactivity could be identified by indirect immunofluorescence. Immunoblot analysis was relatively insensitive, detecting insulin only in the adult Xenopus pancreas. In summary, insulin (from maternal origin and embryonic expression) appears to be present early enough in Xenopus laevis to influence developmental processes such as neurulation. Journal of Endocrinology (1994) 141, 123–129

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45

Gnatenko, D. A., E. P. Kopantsev, and E. D. Sverdlov. "Role of fibroblast growth factors in pancreatic cancer." Biomeditsinskaya Khimiya 62, no. 6 (2016): 622–29. http://dx.doi.org/10.18097/pbmc20166206622.

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Fibroblast growth factors belong to a family of growth factors that are involved in various processes in organism and have a wide range of biological functions. Specifically for pancreas, FGFs are important during both organogenesis and carcinogenesis. One of the main characteristic of pancreatic cancer, is it close interaction between cancer and stromal cells via different factors, including FGF. Pathological changes in FGF/FGFR signaling pathway is a complex process. The remodeling effects and stimulation of tumor growth are mostly depend not only on types of receptors, but also from their isoforms. FGF/FGFR signaling pathway is a perspective specific marker for cancer progression, and a potential drug target, which can be used for treatment of pancreatic cancer.

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46

Pan, F. C., E. D. Bankaitis, D. Boyer, X. Xu, M. Van de Casteele, M. A. Magnuson, H. Heimberg, and C. V. E. Wright. "Spatiotemporal patterns of multipotentiality in Ptf1a-expressing cells during pancreas organogenesis and injury-induced facultative restoration." Development 140, no. 4 (January 16, 2013): 751–64. http://dx.doi.org/10.1242/dev.090159.

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47

Beccaria, C., J. P. Diaz, R. Connes, and B. Chatain. "Organogenesis of the exocrine pancreas in the sea bass, Dicentrarchus labrax L., reared extensively and intensively." Aquaculture 99, no. 3-4 (December 1991): 339–54. http://dx.doi.org/10.1016/0044-8486(91)90254-5.

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48

Ramalho-Santos, M., D. A. Melton, and A. P. McMahon. "Hedgehog signals regulate multiple aspects of gastrointestinal development." Development 127, no. 12 (June 15, 2000): 2763–72. http://dx.doi.org/10.1242/dev.127.12.2763.

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The gastrointestinal tract develops from the embryonic gut, which is composed of an endodermally derived epithelium surrounded by cells of mesodermal origin. Cell signaling between these two tissue layers appears to play a critical role in coordinating patterning and organogenesis of the gut and its derivatives. We have assessed the function of Sonic hedgehog and Indian hedgehog genes, which encode members of the Hedgehog family of cell signals. Both are expressed in gut endoderm, whereas target genes are expressed in discrete layers in the mesenchyme. It was unclear whether functional redundancy between the two genes would preclude a genetic analysis of the roles of Hedgehog signaling in the mouse gut. We show here that the mouse gut has both common and separate requirements for Sonic hedgehog and Indian hedgehog. Both Sonic hedgehog and Indian hedgehog mutant mice show reduced smooth muscle, gut malrotation and annular pancreas. Sonic hedgehog mutants display intestinal transformation of the stomach, duodenal stenosis (obstruction), abnormal innervation of the gut and imperforate anus. Indian hedgehog mutants show reduced epithelial stem cell proliferation and differentiation, together with features typical of Hirschsprung's disease (aganglionic colon). These results show that Hedgehog signals are essential for organogenesis of the mammalian gastrointestinal tract and suggest that mutations in members of this signaling pathway may be involved in human gastrointestinal malformations.

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49

Willmann, Stefanie J. "Gene Expression Profiling of the Mouse Pancreas during the Secondary Transition in the Organogenesis of the Pancreatic Gland*." Journal of Diabetes Mellitus 11, no. 01 (2021): 1–9. http://dx.doi.org/10.4236/jdm.2021.111001.

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50

Kawaguchi, Yoshiya, Kyoichi Takaori, and Shinji Uemoto. "Genetic lineage tracing, a powerful tool to investigate the embryonic organogenesis and adult organ maintenance of the pancreas." Journal of Hepato-Biliary-Pancreatic Sciences 18, no. 1 (July 29, 2010): 1–5. http://dx.doi.org/10.1007/s00534-010-0307-z.

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