Epithelial-to-mesenchymal transition in cyst lining epithelial cells in an orthologous PCK rat model of autosomal-recessive polycystic kidney disease.

@article{Togawa2011EpithelialtomesenchymalTI,
  title={Epithelial-to-mesenchymal transition in cyst lining epithelial cells in an orthologous PCK rat model of autosomal-recessive polycystic kidney disease.},
  author={Hiroko Togawa and Koichi Nakanishi and Hironobu Mukaiyama and Taketsugu Hama and Yuko Shima and Mayumi Sako and Masayasu Miyajima and Kandai Nozu and Kazuhiro Nishii and Shizuko Nagao and Hisahide Takahashi and Kazumoto Iijima and Norishige Yoshikawa},
  journal={American journal of physiology. Renal physiology},
  year={2011},
  volume={300 2},
  pages={
          F511-20
        }
}
In polycystic kidney disease (PKD), cyst lining cells show polarity abnormalities. Recent studies have demonstrated loss of cell contact in cyst cells, suggesting induction of epithelial-to-mesenchymal transition (EMT). Recently, EMT has been implicated in the pathogenesis of PKD. To explore further evidence of EMT in PKD, we examined age- and segment-specific expression of adhesion molecules and mesenchymal markers in PCK rats, an orthologous model of human autosomal-recessive PKD. Kidneys… 

Aberrant Smad3 phosphoisoforms in cyst-lining epithelial cells in the cpk mouse, a model of autosomal recessive polycystic kidney disease.

A qualitative rather than a quantitative abnormality of the TGF-β/Smad3 pathway is involved in PKD and may be a target for disease-specific intervention.

Aberrant expression of laminin-332 promotes cell proliferation and cyst growth in ARPKD.

It is demonstrated that laminin-332 is aberrantly expressed in cysts and precystic tubules of human autosomal recessive PKD kidneys as well as in the kidneys of PCK rats, an orthologous ARPKD model, and abnormal expression of laminIn-332 contributes to the aberrant proliferation of cyst epithelial cells and cyst growth in genetic forms of PKD.

Periostin overexpression in collecting ducts accelerates renal cyst growth and fibrosis in polycystic kidney disease.

It is found that periostin increased gene expression of pathways involved in repair, including integrin and growth factor signaling and ECM production, and it stimulated focal adhesion kinase, Rho GTPase, cytoskeletal reorganization and migration of PKD cells.

Expression of Focal Adhesion Proteins in the Developing Rat Kidney

The temporospatially regulated expression of focal adhesion proteins during kidney development might play a role in morphogenesis and cell differentiation.

Reduction of ciliary length through pharmacologic or genetic inhibition of CDK5 attenuates polycystic kidney disease in a model of nephronophthisis

The data support therapeutic approaches aimed at restoration of ciliogenesis and cellular differentiation as a promising strategy for the treatment of renal cystic diseases and suggest that CDK5 may regulate ciliary length by affecting tubulin dynamics via its substrate collapsin response mediator protein 2.

Extracellular matrix, integrins, and focal adhesion signaling in polycystic kidney disease.

Ursolic acid inhibits epithelial–mesenchymal transition by suppressing the expression of astrocyte-elevated gene-1 in human nonsmall cell lung cancer A549 cells

UA inhibited the EMT by suppressing the expression of AEG-1, correlating with inhibition of nuclear factor-&kgr;B in A549 cells, and it may be able to prevent invasion and metastasis of lung cancer cells.

Conditional Mesenchymal Disruption of Pkd1 Results in Osteopenia and Polycystic Kidney Disease

A new model to study abnormalities in bone development and cyst formation in pancreas and kidney caused by Pkd1 gene inactivation is established and evidence for Col1a1(3.6)-Cre mediated deletion of PKd1 in extraskeletal tissues in Col1A1( 3.6-Cre) flox/flox mice is found.

Interaction of G α 12 and Polycystin-1 in Autosomal Dominant Polycystic Kidney Disease

Gα12 is a key signaling molecule for PC1 in the pathogenesis of AD PKD, and inhibition of Gα12 activity could be used as an effective therapeutic target for ADPKD.

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