Fractalkine increases mesangial cell proliferation through reactive oxygen species and mitogen-activated protein kinases

J. Park, K. H. Song, H. Ha

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Mesangial cell proliferation is one of the main features of chronic renal allograft rejection. One unique feature of fractalkine (CX3CL1) is its existence as both a membrane-tethered and a soluble form. Fractalkine expression is increased in acute and chronic allograft rejection. However, its role in mesangial cell proliferation has not yet been clearly explored. Thus, the present study examined whether fractalkine induced mesangial cell proliferation through production of reactive oxygen species (ROS) and activation of mitogen-activated protein kinase (MAPK), two known mediators of mesangial cell proliferation. Growth-arrested and synchronized mouse mesangial cells were stimulated with fractalkine in the presence versus absence of inhibitors against ROS, extracellular signal-regulated protein kinase (ERK), and p38 MAPK. Cell proliferation was assessed by methylthiazoletetrazolium assay, dichlorofluorescein (DCF)-sensitive cellular ROS production by a fluorometer, and MAPK activation by Western blot analysis. Fractalkine (10-50 ng/mL) significantly increased mesangial cell proliferation at 24 hours in a dose-dependent manner, an effect that was abrogated by the ROS and MAPK inhibitors. Fractalkine (50 ng/mL) also induced cellular ROS production and activation of ERK1/2 and p38 MAPK in mesangial cells. These results demonstrated that fractalkine can induce mesangial cell proliferation through production of cellular ROS and activation of MAPK.

Original languageEnglish
Pages (from-to)1026-1028
Number of pages3
JournalTransplantation Proceedings
Volume44
Issue number4
DOIs
StatePublished - May 2012

Bibliographical note

Funding Information:
This work was supported by Ewha Global Top5 Grant 2011 and RP-Grant 2009 ( 2009-1949-1-1 ) from Ewha Womans University to Jehyun Park.

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