Astrocyte and macrophage regulation of YKL-40 expression and cellular response in neuroinflammation

Brain Pathol. 2012 Jul;22(4):530-46. doi: 10.1111/j.1750-3639.2011.00550.x. Epub 2011 Dec 22.


Numerous inflammatory conditions are associated with elevated YKL-40 expression by infiltrating macrophages. Thus, we were surprised to observe minimal macrophage and abundant astrocyte expression of YKL-40 in neuroinflammatory conditions. The aims of the current study were to better delineate this discrepancy, characterize the factors that regulate YKL-40 expression in macrophages and astrocytes and study whether YKL-40 expression correlates with cell morphology and/or activation state. In vitro, macrophages expressed high levels of YKL-40 that was induced by classical activation and inhibited by alternative activation. Cytokines released from macrophages induced YKL-40 transcription in astrocytes that was accompanied by morphological changes and altered astrocytic motility. Because coculturing of astrocytes and macrophages did not reverse this in vitro expression pattern, additional components of the in vivo central nervous system (CNS) milieu must be required to suppress macrophage and induce astrocyte expression of YKL-40.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipokines / biosynthesis*
  • Astrocytes / metabolism*
  • Blotting, Western
  • Brain / metabolism*
  • Brain / pathology
  • Chitinase-3-Like Protein 1
  • Coculture Techniques
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Humans
  • In Situ Hybridization
  • Inflammation / metabolism
  • Inflammation / pathology
  • Lectins / biosynthesis*
  • Macrophages / metabolism*
  • Real-Time Polymerase Chain Reaction


  • Adipokines
  • CHI3L1 protein, human
  • Chitinase-3-Like Protein 1
  • Lectins