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  • American Physiological Society  (4)
  • 2005-2009  (4)
  • 1
    Online Resource
    Online Resource
    Hypoxia stimulates pancreatic stellate cells to induce fibrosis and angiogenesis in pancreatic cancer
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 295, No. 4 ( 2008-10), p. G709-G717
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 295, No. 4 ( 2008-10), p. G709-G717
    Abstract: Pancreatic cancer is characterized by excessive desmoplastic reaction and by a hypoxic microenvironment within the solid tumor mass. Chronic pancreatitis is also characterized by fibrosis and hypoxia. Fibroblasts in the area of fibrosis in these pathological settings are now recognized as activated pancreatic stellate cells (PSCs). Recent studies have suggested that a hypoxic environment concomitantly exists not only in pancreatic cancer cells but also in surrounding PSCs. This study aimed to clarify whether hypoxia affected the cell functions in PSCs. Human PSCs were isolated and cultured under normoxia (21% O 2 ) or hypoxia (1% O 2 ). We examined the effects of hypoxia and conditioned media of hypoxia-treated PSCs on cell functions in PSCs and in human umbilical vein endothelial cells. Hypoxia induced migration, type I collagen expression, and vascular endothelial growth factor (VEGF) production in PSCs. Conditioned media of hypoxia-treated PSCs induced migration of PSCs, which was inhibited by anti-VEGF antibody but not by antibody against hepatocyte growth factor. Conditioned media of hypoxia-treated PSCs induced endothelial cell proliferation, migration, and angiogenesis in vitro and in vivo. PSCs expressed several angiogenesis-regulating molecules including VEGF receptors, angiopoietin-1, and Tie-2. In conclusion, hypoxia induced profibrogenic and proangiogenic responses in PSCs. In addition to their established profibrogenic roles, PSCs might play proangiogenic roles during the development of pancreatic fibrosis, where they are subjected to hypoxia.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.90356.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Bone marrow contributes to the population of pancreatic stellate cells in mice
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 297, No. 6 ( 2009-12), p. G1138-G1146
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 297, No. 6 ( 2009-12), p. G1138-G1146
    Abstract: Activated pancreatic stellate cells (PSCs) play a pivotal role in the development of pancreatic fibrosis. The origin of activated PSCs has been thought to be transformation of quiescent PSCs residing locally in the pancreas. Recent studies have suggested that bone marrow (BM)-derived cells participate in regeneration processes in various organs. This study aimed to clarify the contribution of BM-derived cells to the population of PSCs in mice. We transplanted BM cells from male enhanced green fluorescent protein transgenic mice into female C57BL/6 mice after lethal irradiation. Eight weeks after BM transplantation, chronic pancreatitis was induced by administration of six intra-abdominal injections of cerulein (50 μg/kg body wt) at 1-h intervals, 3 days per week, for the total of 6 wk. BM-derived cells were tracked by green fluorescent protein expression and in situ hybridization for the Y-chromosome. Eight weeks after BM transplantation, BM-derived cells accounted for 8.7% of the desmin (a marker of PSCs)-positive cells in the pancreas. We could isolate BM-derived cells, which contained lipid droplets and expressed desmin. They could be transformed to myofibroblast-like cells by culture in vitro, further supporting that BM contributed to the population of quiescent PSCs. After induction of pancreatic fibrosis, BM-derived cells accounted for 20.2% of α-smooth muscle actin-positive activated PSCs. The contribution of BM-derived cells to pancreatic ductal cells (positive for cytokeratin-19) was rare and less than 1%. In conclusion, our results suggested that BM-derived cells contributed to the population of PSCs in mice.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00123.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Comprehensive analysis of the ascidian genome reveals novel insights into the molecular evolution of ion channel genes
    American Physiological Society ; 2005
    In:  Physiological Genomics Vol. 22, No. 3 ( 2005-08-11), p. 269-282
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 22, No. 3 ( 2005-08-11), p. 269-282
    Abstract: Ion fluxes through membrane ion channels play crucial roles both in neuronal signaling and the homeostatic control of body electrolytes. Despite our knowledge about the respective ion channels, just how diversification of ion channel genes underlies adaptation of animals to the physical environment remains unknown. Here we systematically survey up to 160 putative ion channel genes in the genome of Ciona intestinalis and compare them with corresponding gene sets from the genomes of the nematode Chaenorhabditis elegans, the fruit fly Drosophila melanogaster, and the more closely related genomes of vertebrates. Ciona has a set of so-called “prototype” genes for ion channels regulating neuronal excitability, or for neurotransmitter receptors, suggesting that genes responsible for neuronal signaling in mammals appear to have diversified mainly via gene duplications of the more restricted members of ancestral genomes before the ascidian/vertebrate divergence. Most genes responsible for modulation of neuronal excitability and pain sensation are absent from the ascidian genome, suggesting that these genes arose after the divergence of urochordates. In contrast, the divergent genes encoding connexins, transient receptor potential-related channels and chloride channels, channels involved rather in homeostatic control, indicate gene duplication events unique to the ascidian lineage. Because several invertebrate-unique channel genes exist in Ciona genome, the crown group of extant vertebrates not only acquired novel channel genes via gene/genome duplications but also discarded some ancient genes that have persisted in invertebrates. Such genome-wide information of ion channel genes in basal chordates enables us to begin correlating the innovation and remodeling of genes with the adaptation of more recent chordates to their physical environment.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00229.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 2031330-5
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  • 4
    Online Resource
    Online Resource
    NADPH oxidase plays a crucial role in the activation of pancreatic stellate cells
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 294, No. 1 ( 2008-01), p. G99-G108
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 294, No. 1 ( 2008-01), p. G99-G108
    Abstract: 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 (p22 phox , p47 phox , NOX1, gp91 phox /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.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00272.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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