BROWSE

Related Researcher

Author

Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

ITEM VIEW & DOWNLOAD

Intestinal Epithelial Cell-Specific Deletion of PLD2 Alleviates DSS-Induced Colitis by Regulating Occludin

Cited 0 times inthomson ciCited 0 times inthomson ci
Title
Intestinal Epithelial Cell-Specific Deletion of PLD2 Alleviates DSS-Induced Colitis by Regulating Occludin
Author
Chelakkot, ChaithanyaGhim, JaewangRajasekaran, NirmalChoi, Jong-SunKim, Jung-HwanJang, Myoung HoShin, Young KeeSuh, Pann-GhillRyu, Sung Ho
Keywords
Mechanisms of disease;  Ulcerative colitis
Issue Date
201705
Publisher
NATURE PUBLISHING GROUP
Citation
SCIENTIFIC REPORTS, v.7, no., pp.1573 -
Abstract
Ulcerative colitis is a multi-factorial disease involving a dysregulated immune response. Disruptions to the intestinal epithelial barrier and translocation of bacteria, resulting in inflammation, are common in colitis. The mechanisms underlying epithelial barrier dysfunction or regulation of tight junction proteins during disease progression of colitis have not been clearly elucidated. Increase in phospholipase D (PLD) activity is associated with disease severity in colitis animal models. However, the role of PLD2 in the maintenance of intestinal barrier integrity remains elusive. We have generated intestinal specific Pld2 knockout mice (Pld2 IEC-KO) to investigate the mechanism of intestinal epithelial PLD2 in colitis. We show that the knockout of Pld2 confers protection against dextran sodium sulphate (DSS)-induced colitis in mice. Treatment with DSS induced the expression of PLD2 and downregulated occludin in colon epithelial cells. PLD2 was shown to mediate phosphorylation of occludin and induce its proteasomal degradation in a c-Src kinase-dependent pathway. Additionally, we have shown that treatment with an inhibitor of PLD2 can rescue mice from DSS-induced colitis. To our knowledge, this is the first report showing that PLD2 is pivotal in the regulation of the integrity of epithelial tight junctions and occludin turn over, thereby implicating it in the pathogenesis of colitis.
URI
Go to Link
DOI
http://dx.doi.org/10.1038/s41598-017-01797-y
ISSN
2045-2322
Appears in Collections:
SLS_Journal Papers
Files in This Item:
2-s2.0-85019227430.pdfDownload

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record

qr_code

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU