RGD Reference Report - IFN-inducible protein-10 plays a pivotal role in maintaining slit-diaphragm function by regulating podocyte cell-cycle balance. - Rat Genome Database

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IFN-inducible protein-10 plays a pivotal role in maintaining slit-diaphragm function by regulating podocyte cell-cycle balance.

Authors: Han, GD  Suzuki, K  Koike, H  Suzuki, K  Yoneyama, H  Narumi, S  Shimizu, F  Kawachi, H 
Citation: Han GD, etal., J Am Soc Nephrol. 2006 Feb;17(2):442-53. Epub 2005 Dec 28.
RGD ID: 2311386
Pubmed: PMID:16382022   (View Abstract at PubMed)
DOI: DOI:10.1681/ASN.2004090755   (Journal Full-text)

IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was reported recently to have several additional biologic activities. In this study, the pathophysiologic role of IP-10 in the glomerular visceral epithelial cell (podocyte) was investigated. In cultured podocytes subjected to recombinant IP-10 treatment, the expression of slit-diaphragm (SD) components nephrin and podocin clearly was heightened. Rats that had puromycin aminonucleoside nephropathy and anti-nephrin antibody-induced nephropathy and were subjected to anti-IP-10 function-blocking antibody (anti-IP-10 mAb) treatment displayed a decrease in the protein level of SD components, as well as exacerbated proteinuria. For exploration of the mechanisms of this process, the interaction between IP-10 and the cell-cycle regulatory proteins was investigated. Cultured podocytes subjected to recombinant IP-10 treatment displayed an increase in the protein level of p27(Kip1), whereas the levels of cyclins E and A decreased. The expression of IP-10 and SD components was heightened by the treatment of siRNA of cyclin A, whereas these expressions were lowered by the treatment of siRNA of p27(Kip1). Proteinuric rats subjected to anti-IP-10 mAb treatment displayed a heightened expression of cyclin A from the early phase of the disease, which indicates that the anti-IP-10 mAb treatment exacerbates podocyte injury by disturbing the cell-cycle balance. These results raise the possibility that IP-10 could become a novel therapeutic target in nephrotic syndrome and several diseases with altered cell-cycle balance.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
CXCL10Humanproteinuria  ISORGD:620209 RGD 
Cxcl10Ratproteinuria  IMP  RGD 
Cxcl10Mouseproteinuria  ISORGD:620209 RGD 


Genes (Rattus norvegicus)
Cxcl10  (C-X-C motif chemokine ligand 10)

Genes (Mus musculus)
Cxcl10  (C-X-C motif chemokine ligand 10)

Genes (Homo sapiens)
CXCL10  (C-X-C motif chemokine ligand 10)