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Surgical injury to the mouse pancreas through ligation of the pancreatic duct as a model for endocrine and exocrine reprogramming and proliferation

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Abstract
Expansion of pancreatic beta cells in vivo or ex vivo, or generation of beta cells by differentiation from an embryonic or adult stem cell, can provide new expandable sources of beta cells to alleviate the donor scarcity in human islet transplantation as therapy for diabetes. Although recent advances have been made towards this aim, mechanisms that regulate beta cell expansion and differentiation from a stem/progenitor cell remain to be characterized. Here, we describe a protocol for an injury model in the adult mouse pancreas that can function as a tool to study mechanisms of tissue remodeling and beta cell proliferation and differentiation. Partial duct ligation (PDL) is an experimentally induced injury of the rodent pancreas involving surgical ligation of the main pancreatic duct resulting in an obstruction of drainage of exocrine products out of the tail region of the pancreas. The inflicted damage induces acinar atrophy, immune cell infiltration and severe tissue remodeling. We have previously reported the activation of Neurogenin (Ngn) 3 expressing endogenous progenitor-like cells and an increase in beta cell proliferation after PDL. Therefore, PDL provides a basis to study signals involved in beta cell dynamics and the properties of an endocrine progenitor in adult pancreas. Since, it still remains largely unclear, which factors and pathways contribute to beta cell neogenesis and proliferation in PDL, a standardized protocol for PDL will allow for comparison across laboratories.
Keywords
DIFFERENTIATION, MICE, REGENERATION, PROGENITORS, ISLET GROWTH, ADULT PANCREAS, BETA-CELL NEOGENESIS, CONTRIBUTE, EXPRESSION, INVOLVE, cell reprogramming, cell proliferation, Neurogenin (Ngn) 3, mouse model, cell differentiation, injury, surgery, Partial duct ligation (PDL), Pancreas, Issue 102, Medicine

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Chicago
De Groef, Sofie, Gunter Leuckx, Naomi Van Gassen, Willem Staels, Ying Cai, Yuchi Yuchi, Violette Coppens, et al. 2015. “Surgical Injury to the Mouse Pancreas Through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation.” Jove-journal of Visualized Experiments (102).
APA
De Groef, S., Leuckx, G., Van Gassen, N., Staels, W., Cai, Y., Yuchi, Y., Coppens, V., et al. (2015). Surgical injury to the mouse pancreas through ligation of the pancreatic duct as a model for endocrine and exocrine reprogramming and proliferation. JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, (102).
Vancouver
1.
De Groef S, Leuckx G, Van Gassen N, Staels W, Cai Y, Yuchi Y, et al. Surgical injury to the mouse pancreas through ligation of the pancreatic duct as a model for endocrine and exocrine reprogramming and proliferation. JOVE-JOURNAL OF VISUALIZED EXPERIMENTS. 2015;(102).
MLA
De Groef, Sofie, Gunter Leuckx, Naomi Van Gassen, et al. “Surgical Injury to the Mouse Pancreas Through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation.” JOVE-JOURNAL OF VISUALIZED EXPERIMENTS 102 (2015): n. pag. Print.
@article{6854376,
  abstract     = {Expansion of pancreatic beta cells in vivo or ex vivo, or generation of beta cells by differentiation from an embryonic or adult stem cell, can provide new expandable sources of beta cells to alleviate the donor scarcity in human islet transplantation as therapy for diabetes. Although recent advances have been made towards this aim, mechanisms that regulate beta cell expansion and differentiation from a stem/progenitor cell remain to be characterized. Here, we describe a protocol for an injury model in the adult mouse pancreas that can function as a tool to study mechanisms of tissue remodeling and beta cell proliferation and differentiation. Partial duct ligation (PDL) is an experimentally induced injury of the rodent pancreas involving surgical ligation of the main pancreatic duct resulting in an obstruction of drainage of exocrine products out of the tail region of the pancreas. The inflicted damage induces acinar atrophy, immune cell infiltration and severe tissue remodeling. We have previously reported the activation of Neurogenin (Ngn) 3 expressing endogenous progenitor-like cells and an increase in beta cell proliferation after PDL. Therefore, PDL provides a basis to study signals involved in beta cell dynamics and the properties of an endocrine progenitor in adult pancreas. Since, it still remains largely unclear, which factors and pathways contribute to beta cell neogenesis and proliferation in PDL, a standardized protocol for PDL will allow for comparison across laboratories.},
  articleno    = {e52765},
  author       = {De Groef, Sofie and Leuckx, Gunter and Van Gassen, Naomi and Staels, Willem and Cai, Ying and Yuchi, Yuchi and Coppens, Violette and De Leu, Nico and Heremans, Yves and Baeyens, Luc and Van de Casteele, Mark and Heimberg, Harry},
  issn         = {1940-087X},
  journal      = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
  keyword      = {DIFFERENTIATION,MICE,REGENERATION,PROGENITORS,ISLET GROWTH,ADULT PANCREAS,BETA-CELL NEOGENESIS,CONTRIBUTE,EXPRESSION,INVOLVE,cell reprogramming,cell proliferation,Neurogenin (Ngn) 3,mouse model,cell differentiation,injury,surgery,Partial duct ligation (PDL),Pancreas,Issue 102,Medicine},
  language     = {eng},
  number       = {102},
  pages        = {9},
  title        = {Surgical injury to the mouse pancreas through ligation of the pancreatic duct as a model for endocrine and exocrine reprogramming and proliferation},
  url          = {http://dx.doi.org/10.3791/52765},
  year         = {2015},
}

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