Hypoxia activates pancreatic stellate cells: Development of an organotypic culture model of thick slices of normal human pancreas

Pancreatology ◽  
2012 ◽  
Vol 12 (6) ◽  
pp. 588
Author(s):  
V. Rebours ◽  
M. Albuquerque ◽  
P. Ruszniewski ◽  
A. Sauvanet ◽  
V. Paradis ◽  
...  
Keyword(s):  
Organotypic Culture ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreas ◽  
Culture Model ◽  
Normal Human

870 Hypoxia Activates Pancreatic Stellate Cells: Development of an Organotypic Culture Model of Thick Slices of Normal Human Pancreas

2012 ◽  
Vol 142 (5) ◽  
pp. S-150
Author(s):  
Vinciane Rebours ◽  
Miguel Albuquerque ◽  
Philippe B. Ruszniewski ◽  
Alain Sauvanet ◽  
Valérie Paradis ◽  
...  
Keyword(s):  
Organotypic Culture ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreas ◽  
Culture Model ◽  
Normal Human

scholarly journals Hypoxia Pathways and Cellular Stress Activate Pancreatic Stellate Cells: Development of an Organotypic Culture Model of Thick Slices of Normal Human Pancreas

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76229 ◽  
Author(s):  
Vinciane Rebours ◽  
Miguel Albuquerque ◽  
Alain Sauvanet ◽  
Philippe Ruszniewski ◽  
Philippe Lévy ◽  
...  
Keyword(s):  
Organotypic Culture ◽  
Cellular Stress ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreas ◽  
Culture Model ◽  
Normal Human

Identification of markers for quiescent pancreatic stellate cells in the normal human pancreas

2017 ◽  
Vol 148 (4) ◽  
pp. 359-380 ◽  
Author(s):  
Michael Friberg Bruun Nielsen ◽  
Michael Bau Mortensen ◽  
Sönke Detlefsen
Keyword(s):  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreas ◽  
Normal Human

Pancreatic stellate cells increase cancer cell expression of HMGA2 in a 3D co-culture model of pancreatic cancer

Pancreatology ◽  
2017 ◽  
Vol 17 (3) ◽  
pp. S34
Author(s):  
Jessica Norberg ◽  
Carina Strell ◽  
Andrea Balboni ◽  
Arne Östman ◽  
Rainer Heuchel ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cell ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Culture Model ◽  
Cell Expression

NADPH oxidase plays a crucial role in the activation of pancreatic stellate cells

2008 ◽  
Vol 294 (1) ◽  
pp. G99-G108 ◽  
Author(s):  
Atsushi Masamune ◽  
Takashi Watanabe ◽  
Kazuhiro Kikuta ◽  
Kennichi Satoh ◽  
Tooru Shimosegawa
Keyword(s):  
Chronic Pancreatitis ◽  
Nadph Oxidase ◽  
Stellate Cells ◽  
Pancreatic Fibrosis ◽  
Pancreatic Stellate Cells ◽  
Human Pancreas ◽  
Ros Production ◽  
Chemokine Production ◽  
Cell Functions ◽  
Diphenylene Iodonium

Activated pancreatic stellate cells (PSCs) play an important role in pancreatic fibrosis and inflammation, where oxidative stress is implicated in the pathogenesis. NADPH oxidase might be a source of reactive oxygen species (ROS) in the injured pancreas. This study aimed to clarify the expression and regulation of cell functions by NADPH oxidase in PSCs. PSCs were isolated from rat and human pancreas tissues. Expression of NADPH oxidase was assessed by reverse transcription-PCR and immunostaining. Intracellular ROS production was assessed using 2′,7′-dichlorofluorescin diacetate. The effects of diphenylene iodonium (DPI) and apocynin, inhibitors of NADPH oxidase, on key parameters of PSC activation were evaluated in vitro. In vivo, DPI (at 1 mg·kg body wt−1·day−1) was administered in drinking water to 10-wk-old male Wistar Bonn/Kobori rats for 10 wk and to rats with chronic pancreatitis induced by dibutyltin dichloride (DBTC). PSCs expressed key components of NADPH oxidase (p22phox, p47phox, NOX1, gp91phox/NOX2, NOX4, and NOX activator 1). PDGF-BB, IL-1β, and angiotensin II induced ROS production, which was abolished by DPI and apocynin. DPI inhibited PDGF-induced proliferation, IL-1β-induced chemokine production, and expression of α-smooth muscle actin and collagen. DPI inhibited transformation of freshly isolated cells to a myofibroblast-like phenotype. In addition, DPI inhibited the development of pancreatic fibrosis in Wistar Bonn/Kobori rats and in rats with DBTC-induced chronic pancreatitis. In conclusion, PSCs express NADPH oxidase to generate ROS, which mediates key cell functions and activation of PSCs. NADPH oxidase might be a potential target for the treatment of pancreatic fibrosis.

ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCREATIC STELLATE CELLS (HPSCS)

Pancreas ◽  
2007 ◽  
Vol 35 (4) ◽  
pp. 433-434
Author(s):  
A. Vonlaufen ◽  
Z. Xu ◽  
L. Yang ◽  
Biankin ◽  
N. Parker ◽  
...  
Keyword(s):  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Normal Human

scholarly journals Activation of Pancreatic Stellate Cells Is Beneficial for Exocrine but Not Endocrine Cell Differentiation in the Developing Human Pancreas

2021 ◽  
Vol 9 ◽  
Author(s):  
Jinming Li ◽  
Bijun Chen ◽  
George F. Fellows ◽  
Cynthia G. Goodyer ◽  
Rennian Wang
Keyword(s):  
Cell Differentiation ◽  
Beta Cell ◽  
Islet Cell ◽  
Stellate Cell ◽  
Stellate Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Stellate Cells ◽  
Small Subset ◽  
Human Pancreas ◽  
Pancreatic Development

Pancreatic stellate cells (PaSCs) are non-endocrine, mesenchymal-like cells that reside within the peri-pancreatic tissue of the rodent and human pancreas. PaSCs regulate extracellular matrix (ECM) turnover in maintaining the integrity of pancreatic tissue architecture. Although there is evidence indicating that PaSCs are involved in islet cell survival and function, its role in islet cell differentiation during human pancreatic development remains unclear. The present study examines the expression pattern and functional role of PaSCs in islet cell differentiation of the developing human pancreas from late 1st to 2nd trimester of pregnancy. The presence of PaSCs in human pancreata (8–22 weeks of fetal age) was characterized by ultrastructural, immunohistological, quantitative RT-PCR and western blotting approaches. Using human fetal PaSCs derived from pancreata at 14–16 weeks, freshly isolated human fetal islet-epithelial cell clusters (hIECCs) were co-cultured with active or inactive PaSCs in vitro. Ultrastructural and immunofluorescence analysis demonstrated a population of PaSCs near ducts and newly formed islets that appeared to make complex cell-cell dendritic-like contacts. A small subset of PaSCs co-localized with pancreatic progenitor-associated transcription factors (PDX1, SOX9, and NKX6-1). PaSCs were highly proliferative, with significantly higher mRNA and protein levels of PaSC markers (desmin, αSMA) during the 1st trimester of pregnancy compared to the 2nd trimester. Isolated human fetal PaSCs were identified by expression of stellate cell markers and ECM. Suppression of PaSC activation, using all-trans retinoic acid (ATRA), resulted in reduced PaSC proliferation and ECM proteins. Co-culture of hIECCs, directly on PaSCs or indirectly using Millicell® Inserts or using PaSC-conditioned medium, resulted in a reduction the number of insulin+ cells but a significant increase in the number of amylase+ cells. Suppression of PaSC activation or Notch activity during the co-culture resulted in an increase in beta-cell differentiation. This study determined that PaSCs, abundant during the 1st trimester of pancreatic development but decreased in the 2nd trimester, are located near ductal and islet structures. Direct and indirect co-cultures of hIECCs with PaSCs suggest that activation of PaSCs has opposing effects on beta-cell and exocrine cell differentiation during human fetal pancreas development, and that these effects may be dependent on Notch signaling.

IMMUNOLOGICAL REACTIVITY OF INSULIN IN HUMAN SERUM

1966 ◽  
Vol 53 (4) ◽  
pp. 673-680 ◽  
Author(s):  
Torsten Deckert ◽  
Kai R. Jorgensen
Keyword(s):  
Normal Subjects ◽  
The Other ◽  
Human Pancreas ◽  
Porcine Pancreas ◽  
Crystalline Insulin ◽  
Endogenous Insulin ◽  
Significant Difference ◽  
Human Sera ◽  
Normal Human ◽  
The One

ABSTRACT The purpose of this study was to investigate whether a difference could be demonstrated between crystalline insulin extracted from normal human pancreas, and crystalline insulin extracted from bovine and porcine pancreas. Using Hales & Randle's (1963) immunoassay no immunological differences could be demonstrated between human and pig insulin. On the other hand, a significant difference was found, between pig and ox insulin. An attempt was also made to determine whether an immunological difference could be demonstrated between crystalline pig insulin and crystalline human insulin from non diabetic subjects on the one hand and endogenous, circulating insulin from normal subjects, obese subjects and diabetic subjects on the other. No such difference was found. From these experiments it is concluded that endogenous insulin in normal, obese and diabetic human sera is immunologically identical with human, crystalline insulin from non diabetic subjects and crystalline pig insulin.

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