Possible involvement of SDF-1α/CXCR4-DPPIV axis in TGF-β1-induced enhancement of migratory potential in human peritoneal mesothelial cells

Hiroaki Kajiyama, Kiyosumi Shibata, Kazuhiko Ino, Akihiro Nawa, Shigehiko Mizutani, Fumitaka Kikkawa

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

We have previously reported that human peritoneal mesothelial cells (HPMCs) express a large amount of dipeptidyl peptidase IV (DPPIV) and that its expression is regulated by a variety of bioactive substances in malignant ascites from ovarian cancer patients. The aim of this study has been to examine the expression and role of the SDF-1α/CXCR4-DPPIV axis in HPMCs. We have demonstrated that the expression levels of DPPIV and E-cadherin in HPMCs decrease, following TGF-β1-induced morphological change, in a time- and concentration-dependent manner. Additionally, we show that both SDF-1α (a chemokine and substrate for DPPIV) and its receptor, CXCR4, are expressed on HPMCs, and that their expression levels are upregulated by TGF-β1 treatment, resulting in an increased migratory potential of HPMCs. Furthermore, the migratory potential of HPMCs is significantly enhanced in the presence of SDF-1α or DPPIV-specific inhibitor in the wound-healing assay. These results suggest that DPPIV and SDF-1α/CXCR4 play crucial roles in regulating the migratory potential of HPMCs, which may be involved in the re-epithelialization of denuded basement membrane at the site of peritoneal injury.

Original languageEnglish
Pages (from-to)221-229
Number of pages9
JournalCell and Tissue Research
Volume330
Issue number2
DOIs
Publication statusPublished - 01-11-2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Histology
  • Cell Biology

Fingerprint Dive into the research topics of 'Possible involvement of SDF-1α/CXCR4-DPPIV axis in TGF-β1-induced enhancement of migratory potential in human peritoneal mesothelial cells'. Together they form a unique fingerprint.

Cite this