Adiponectin and leptin induce VCAM-1 expression in human and murine chondrocytes

PLoS One. 2012;7(12):e52533. doi: 10.1371/journal.pone.0052533. Epub 2012 Dec 19.

Abstract

Background: Osteoarthritis (OA) and rheumatoid arthritis (RA), the most common rheumatic diseases, are characterized by irreversible degeneration of the joint tissues. There are several factors involved in the pathogenesis of these diseases including pro-inflammatory cytokines, adipokines and adhesion molecules.

Objective: Up to now, the relationship between adipokines and adhesion molecules at cartilage level was not explored. Thus, the aim of this article was to study the effect of leptin and adiponectin on the expression of VCAM-1 in human and murine chondrocytes. For completeness, intracellular signal transduction pathway was also explored.

Methods: VCAM-1 expression was assessed by quantitative RT-PCR and western blot analysis upon treatment with leptin, adiponectin and other pertinent reagents in cultured human primary chondrocytes. Signal transduction pathways have been explored by using specific pharmacological inhibitors in the adipokine-stimulated human primary chondrocytes and ATDC5 murine chondrocyte cell line.

Results: Herein, we demonstrate, for the first time, that leptin and adiponectin increase VCAM-1 expression in human and murine chondrocytes. In addition, both adipokines have additive effect with IL-1β. Finally, we demonstrate that several kinases, including JAK2, PI3K and AMPK are at a play in the intracellular signalling of VCAM-1 induction.

Conclusions: Taken together, our results suggest that leptin and adiponectin could perpetuate cartilage-degrading processes by inducing also factors responsible of leukocyte and monocyte infiltration at inflamed joints.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / pharmacology*
  • Animals
  • Blotting, Western
  • Cell Line
  • Chondrocytes / drug effects
  • Chondrocytes / metabolism*
  • Humans
  • Leptin / pharmacology*
  • Mice
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Signal Transduction / genetics
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism*

Substances

  • Adiponectin
  • Leptin
  • RNA, Messenger
  • Vascular Cell Adhesion Molecule-1

Grants and funding

The work of O.G. and F.L. is funded by the Instituto de Salud Carlos III and the Xunta de Galicia (SERGAS) through a research-staff stabilization contract. O.G. is supported by Instituto de Salud Carlos III and Xunta de Galicia. This work was also partially supported by RETICS Program, RD08/0075 (RIER) from Instituto de Salud Carlos III (ISCIII), within the VI NP of R+D+I 2008–2011. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.