Role of CIP4 in high glucose induced epithelial--mesenchymal transition of rat peritoneal mesothelial cells

@article{Zhang2013RoleOC,
  title={Role of CIP4 in high glucose induced epithelial--mesenchymal transition of rat peritoneal mesothelial cells},
  author={J. Zhang and Meisheng Bi and Feng Zhong and Xuelong Jiao and Dianliang Zhang and Qian Dong},
  journal={Renal Failure},
  year={2013},
  volume={35},
  pages={989 - 995}
}
Abstract Background: Peritoneal mesothelial cell (PMC) plays a key role in the process of peritoneal fibrosis. Epithelial–mesenchymal transition (EMT) of PMCs is an important mechanism of peritoneal fibrosis. Prolonged exposure to peritoneal dialysis fluid containing a high concentration of glucose may lead to EMT of PMCs. Cdc42-interacting protein-4 (CIP4) is a critical regulator of cell skeleton and downstream effector of Cdc42 and participates in EMT of tubular epithelial cells. In the… Expand
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References

SHOWING 1-10 OF 34 REFERENCES
HGF and BMP-7 ameliorate high glucose-induced epithelial-to-mesenchymal transition of peritoneal mesothelium.
TLDR
It is found that high concentrations of glucose induced epithelial-to-mesenchymal transition (EMT) of HPMC, suggested by decreased expression of E-cadherin and increased expression of alpha-smooth muscle actin, fibronectin, and type I collagen and by increased cell migration, is induced. Expand
Characterization of Epithelial-to-Mesenchymal Transition of Mesothelial Cells in a Mouse Model of Chronic Peritoneal Exposure to High Glucose Dialysate
  • L. Aroeira, J. Loureiro, +7 authors R. Selgas
  • Medicine
  • Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis
  • 2008
TLDR
It is demonstrated that epithelial-to-mesenchymal transition (EMT) of mesothelial cells takes place in mouse peritoneum exposed to PDF, validating this model for the study of effects of drugs on the EMT process as a therapy for peritoneal deterioration. Expand
BMP-7 blocks mesenchymal conversion of mesothelial cells and prevents peritoneal damage induced by dialysis fluid exposure.
  • J. Loureiro, M. Schilte, +12 authors M. López-Cabrera
  • Medicine
  • Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 2010
TLDR
Data point to a balance between BMP-7 and TGF-beta1 in the control of EMT and indicate that blockade of E MT may be a therapeutic approach to ameliorate peritoneal membrane damage during PD. Expand
Effect of High Glucose on Peritoneal Mesothelial Cell Biology
  • H. Ha, H. B. Lee
  • Medicine
  • Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis
  • 2000
TLDR
ROS, recently recognized as signalling molecules, are rapidly generated in HPMC as a result of increased glucose metabolism and may prove to be an important mediator of HG-induced peritoneal injury. Expand
Cdc42-Interacting Protein-4 Promotes TGF-Β1-Induced Epithelial-Mesenchymal Transition and Extracellular Matrix Deposition in Renal Proximal Tubular Epithelial Cells
TLDR
Results of the current study suggest that CIP4 promotes TGF-β1-induced EMT in tubular epithelial cells, and is capable of inducing ECM deposition and exacerbating progressive fibrosis in chronic renal failure. Expand
Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention.
  • Youhua Liu
  • Medicine, Biology
  • Journal of the American Society of Nephrology : JASN
  • 2004
TLDR
A comprehensive review of recent advances on understanding the pathologic significance, molecular mechanism, and therapeutic intervention of EMT in the setting of chronic renal fibrosis is provided. Expand
Basic Mechanisms and Clinical Implications of Peritoneal Fibrosis
  • P. Margetts, P. Bonniaud
  • Medicine
  • Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis
  • 2003
TLDR
The role of certain growth factors and cytokines in peritoneal fibrosis, including TGFbeta, TIMP-1, and inflammatory cytokines, especially IL-1beta, have been stressed, and the induction of angiogenesis has been focused on, as this appears to correlate with increased solute transport andperitoneal membrane ultrafiltration failure. Expand
Peroxisome Proliferator-Activated Receptor-Gamma Is Expressed by Rat Peritoneal Mesothelial Cells: Its Potential Role in Peritoneal Cavity Local Defense
TLDR
There is constitutive expression ofPPARγ in cultured RPMCs and PPARγ ligands which strongly inhibit LPS-induced CD40 and ICAM-1 production in RPMCs, suggesting that PPARα might play a part in the local defense of the peritoneal cavity by downregulating inflammatory mediators. Expand
Troglitazone ameliorates high glucose-induced EMT and dysfunction of SGLTs through PI3K/Akt, GSK-3β, Snail1, and β-catenin in renal proximal tubule cells.
  • Yu Jin Lee, H. Han
  • Chemistry, Medicine
  • American journal of physiology. Renal physiology
  • 2010
TLDR
HG-induced EMT may result in SGLT dysfunction that is restored by the PPARγ agonist troglitazone in primary cultured PTCs and is verified through ROS, PI3K/Akt, GSK-3β, Snail, and β-catenin. Expand
Myofibroblastic conversion of mesothelial cells.
TLDR
It is proposed that differentiated epithelial cells of mesothelium convert or transdifferentiate into myofibroblasts, which implies the recruitment of fibrogenic cells from mesot Helium during serosal inflammation and wound healing. Expand
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