Role of Dlg5/lp-dlg, a Membrane-Associated Guanylate Kinase Family Protein, in Epithelial-Mesenchymal Transition in LLc-PK1 Renal Epithelial Cells

Autor: Kohki Inada, Noriyuki Kioka, Takayuki Sogabe, Lucia Tomiyama, Takuhito Sezaki, Yohsuke Matsuno, Michinori Matsuo, Kumiyo Kakuda, Takafumi Ichikawa, Kazumitsu Ueda
Jazyk: angličtina
Rok vydání: 2012
Předmět:
MAPK signaling cascades
Epithelial-Mesenchymal Transition
Guanylate kinase
Swine
p38 mitogen-activated protein kinases
lcsh:Medicine
Gastroenterology and Hepatology
Membrane-associated guanylate kinase
Signal transduction
Signaling Pathways
p38 Mitogen-Activated Protein Kinases
Molecular cell biology
Transforming Growth Factor beta
Signaling in Cellular Processes
Animals
Epithelial–mesenchymal transition
RNA
Small Interfering
lcsh:Science
Biology
Gene knockdown
Multidisciplinary
biology
lcsh:R
Mechanisms of Signal Transduction
Inflammatory Bowel Disease
JNK Mitogen-Activated Protein Kinases
Signaling cascades
Epithelial Cells
Transforming growth factor beta
Transfection
Cadherins
Molecular biology
Actins
Cell biology
Fibronectins
TGF-beta signaling cascade
biology.protein
Medicine
LLC-PK1 Cells
lcsh:Q
RNA Interference
Cellular Types
Guanylate Kinases
Receptors
Transforming Growth Factor beta
Transforming growth factor
Research Article
Zdroj: PLoS ONE
PLoS ONE, Vol 7, Iss 4, p e35519 (2012)
ISSN: 1932-6203
Popis: Discs large homolog 5 (Dlg5) is a member of the membrane-associated guanylate kinase adaptor family of proteins, some of which are involved in the regulation of epithelial-to-mesenchymal transition (EMT). Dlg5 has been described as a susceptibility gene for Crohn's disease; however, the physiological function of Dlg5 is unknown. We show here that transforming growth factor-β (TGF-β)-induced EMT suppresses Dlg5 expression in LLc-PK1 cells. Depletion of Dlg5 expression by knockdown promoted the expression of the mesenchymal marker proteins, fibronectin and α-smooth muscle actin, and suppressed the expression of E-cadherin. In addition, activation of JNK and p38, which are stimulated by TGF-β, was enhanced by Dlg5 depletion. Furthermore, inhibition of the TGF-β receptor suppressed the effects of Dlg5 depletion. These observations suggest that Dlg5 is involved in the regulation of TGF-βreceptor-dependent signals and EMT.
Databáze: OpenAIRE
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