TITLE

Cell migration: a novel aspect of pancreatic stellate cell biology

AUTHOR(S)
Phillips, P.A.; Wu, M.J.; Kumar, R.K.; Doherty, E.; McCarroll, J.A.; Park, S.; Pirola, R.C.; Wilson, J.S.; Apte, M.V.
PUB. DATE
May 2003
SOURCE
Gut;May2003, Vol. 52 Issue 5, p677
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Pancreatic stellate cells (PSCs), implicated as key mediators of pancreatic fibrogenesis, are found in increased numbers in areas of pancreatic injury. This increase in PSC number may be due to increased local proliferation and/or migration of these cells from adjacent areas. The ability of PSCs to proliferate has been well established but their potential for migration has not been examined. Aims: Therefore, the aims of this study were to determine whether cultured rat PSCs have the capacity to migrate and, if so, to characterise this migratory capacity with respect to the influence of basement membrane components and the effect of platelet derived growth factor (PDGF, a known stimulant for migration of other cell types). Methods: Migration of freshly isolated (quiescent) and culture activated (passaged) rat PSCs was assessed across uncoated or Matrigel (a basement membrane-like substance) coated porous membranes (pore size 8 µm) in the presence or absence of PDGF (10 and 20 ng/ml) in the culture medium. A checkerboard assay was performed to assess whether the effect of PDGF on PSC migration was chemotactic or chemokinetic. Results: Cell migration was observed with both freshly isolated and passaged PSCs. However, compared with passaged (culture activated) cells, migration of freshly isolated cells was delayed, occurring only at or after 48 hours of incubation when the cells displayed an activated phenotype. PSC migration through Matrigel coated membranes was delayed but not prevented by basement membrane components. PSC migration was increased by PDGF and this effect was predominantly chemotactic (that is, in the direction of a positive concentration gradient). Conclusions: (i) PSCs have the capacity to migrate. (ii) Activation of PSCs appears to be a prerequisite for migration. (iii) PDGF stimulates PSC migration and this effect is predominantly chemotactic. Implication: Chemotactic factors released during pancreatic injury may stimulate the...
ACCESSION #
9737019

 

Related Articles

  • Ghrelin Is Present in Pancreatic α-Cells of Humans and Rats and Stimulates Insulin Secretion. Date, Yukari; Nakazato, Masamitsu; Hashiguchi,, Suzuko; Dezaki, Katsuya; Mondal, Muhtashan S.; Hosoda, Hiroshi; Kojima, Masayasu; Kangawa, Kenji; Arima, Terukatsu; Matsuo, Hisayuki; Yada, Toshilfiko; Matsukura, Shigeru // Diabetes;Jan2002, Vol. 51 Issue 1, p124 

    Examines the presence of ghrelin in pancreatic alpha cells of humans and rats. Effects of ghrelin on insulin secretion; Description of growth hormone secretagogues; Cellular source of ghrelin in rat and human pancreas.

  • Molecular basis of transdifferentiation of pancreas to liver. Shen, Chia-Ning; Slack, Jonathan M. W.; Tosh, David // Nature Cell Biology;Dec2000, Vol. 2 Issue 12, p879 

    The appearance of hepatic foci in the pancreas has been described in animal experiments and in human pathology. Here we show that pancreatic cells can be converted into hepatocytes by treatment with a synthetic glucocorticoid, dexamethasone. This occurs both in a pancreatic cell line, AR42J-B13,...

  • Circulating Antibodies Against an Exocrine Pancreatic Enzyme in Type 1 Diabetes. Panicot, Laurence; Mas, Eric; Thivolet, Charles; Lombardo, Dominique // Diabetes;Dec99, Vol. 48 Issue 12, p2316 

    Identifies an autoantigen in type I diabetes originating from the exocrine pancreas. Presence of antibodies to bile salt-dependent lipase (BSDL) in type I diabetic patients; Prevalence of autoreactivity to BSDL in prediabetic and type I diabetic patients; Secretion pathway of BSDL.

  • Localization of the O-Linked N-Acetylglucosamine Transferase in Rat Pancreas. Akimoto, Yoshihiro; Kreppel, Lisa K.; Hirano, Hiroshii; Hart, Gerald W. // Diabetes;Dec99, Vol. 48 Issue 12, p2407 

    Examines the localization of the O-linked N-acetylglucosamine transferase in rat pancreatic cells. Mediation of the hexosamine biosynthesis pathway in the glucose-induced desensitization of the glucose transport system and insulin resistance induction; Elevation of the hexosamine pathway in...

  • Characterization of GPR56 protein and its suppressed expression in human pancreatic cancer cells. Yue Huang; Jun Fan // Molecular & Cellular Biochemistry;Jan2008, Vol. 308 Issue 1/2, p133 

    Abstract  GPR56 is an atypical G protein-coupled receptor (GPCR) with an unusually large N-terminal extracellular region, which contains a long Ser/Thr-rich region forming a mucin-like stalk and due to this feature, GPR56 is thought to be an adhesion GPCR. Recent studies...

  • Late presentation of a mucinous ovarian adenocarcinoma which was initially diagnosed as a primary pancreatic carcinoma: a case report and review of the literature. Sparks, Dorothy A.; Chase, Daniel M.; Forsyth, Mark; Bogen, Gregg; Arnott, Jon // Journal of Medical Case Reports;2010, Vol. 4 Issue 1, p1 

    Introduction: Adenocarcinoma of the ovary is an aggressive neoplasm which often metastasizes to the lung or liver. Metastases rarely occur to the pancreas, but a tissue diagnosis is required to confirm this event. Although most tumors of the pancreas are primary pancreatic neoplasms, metastatic...

  • Pancreatic cancer: Tracing origins. Seton-Rogers, Sarah // Nature Reviews Cancer;Jan2013, Vol. 13 Issue 1, p5 

    The article focuses on pancreatic ductal adenocarcinoma (PDA) which has been used in mouse models for expressing the oncogenic KRAS in pancreatic cells.

  • Pancreatic islet cell autophagy during aging in rats. Shuang Wang; Qian-qian Sun; Bing Xiang; Xiu-Jun Li // Clinical & Investigative Medicine;2013, Vol. 36 Issue 2, pE72 

    Purpose: Autophagy induces pancreatic β cell death. The purpose of the present study was to examine the hypothesis that the extent of pancreatic autophagy is associated with aging and age-related diabetes. Methods: Pancreatic tissue and blood samples were collected from Sprague Dawley rats...

  • Advanced glycation end products impair glucose-induced insulin secretion from rat pancreatic β-cells. Hachiya, Hiroyuki; Miura, Yoshikazu; Inoue, Ken-ichi; Park, Kyung Hwa; Takeuchi, Masayoshi; Kubota, Keiichi // Journal of Hepato -- Biliary -- Pancreatic Sciences;Feb2014, Vol. 21 Issue 2, p134 

    Background Advanced glycation end products ( AGEs) are derivative compounds generated from non-enzymatic glycosylation and oxidation. In comparison with glucose-derived AGEs ( Glu- AGEs), glyceraldehyde-derived AGEs ( Glycer- AGEs) have stronger toxicity to living systems. In this study, we...

Share

Read the Article

Courtesy of VIRGINIA BEACH PUBLIC LIBRARY AND SYSTEM

Sign out of this library

Other Topics