Involvement of growth differentiation factor-15/macrophage inhibitory cytokine-1 (GDF-15/MIC-1) in oxLDL-induced apoptosis of human macrophages in vitro and in arteriosclerotic lesions

Cell Tissue Res. 2004 Nov;318(2):325-33. doi: 10.1007/s00441-004-0986-3. Epub 2004 Oct 1.

Abstract

Growth differentiation factor-15/macrophage inhibitory cytokine-1 (GDF-15/MIC-1) is a new member of the transforming growth factor beta (TGF-beta) superfamily, which has most recently been found in activated macrophages (MPhi). We have now investigated GDF-15/MIC-1 in human MPhi after exposure to oxidized low-density lipoproteins (oxLDL) related mediators in vitro and in arteriosclerotic carotid arteries. Using RT-PCR and Western blotting a pronounced induction of GDF-15/MIC-1 expression by oxLDL, C6-ceramide, tumor necrosis factor (TNFalpha) and hydrogen peroxide (H2O2) was found in cultured human MPhi. In 11 human arteriosclerotic carotid arteries, immunohistochemical analyses supported by computer-assisted morphometry and regression analyses demonstrated a significant colocalization of GDF-15/MIC-1 immunoreactivity (IR) with oxLDL IR and manganese superoxide dismutase (MnSOD) IR in CD68 immunoreactive (ir) MPhi, which were also expressing AIF-IR (apoptosis-inducing factor), caspase-3-IR (CPP32), PARP-IR, c-Jun/AP-1-IR and p53-IR. Our data suggest that GDF-15/MIC-1 is inducible in human MPhi by oxLDL and its mediators in vitro and is supposed to contribute to oxidative stress dependent consequences in arteriosclerotic plaques, e.g. modulating apoptosis and inflammatory processes in activated MPhi.

MeSH terms

  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Apoptosis / drug effects*
  • Apoptosis Inducing Factor
  • Arteriosclerosis / metabolism*
  • Arteriosclerosis / pathology
  • Bone Morphogenetic Proteins / biosynthesis*
  • Bone Morphogenetic Proteins / genetics
  • Carotid Arteries / metabolism
  • Carotid Artery Diseases / metabolism
  • Carotid Artery Diseases / pathology
  • Caspase 3
  • Caspases / metabolism
  • Cells, Cultured
  • Ceramides / pharmacology
  • Collagen Type XI / metabolism
  • Flavoproteins / metabolism
  • Growth Differentiation Factor 15
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Image Processing, Computer-Assisted / methods
  • Lipoproteins, LDL / metabolism
  • Lipoproteins, LDL / pharmacology*
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Macrophages / pathology
  • Membrane Proteins / biosynthesis*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Oxidative Stress
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • Proto-Oncogene Proteins c-jun / metabolism
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • AIFM1 protein, human
  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • Apoptosis Inducing Factor
  • Bone Morphogenetic Proteins
  • CD68 antigen, human
  • COL11A2 protein, human
  • Ceramides
  • Collagen Type XI
  • Flavoproteins
  • GDF15 protein, human
  • Growth Differentiation Factor 15
  • Lipoproteins, LDL
  • Membrane Proteins
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • oxidized low density lipoprotein
  • N-caproylsphingosine
  • Hydrogen Peroxide
  • Superoxide Dismutase
  • PARP1 protein, human
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • CASP3 protein, human
  • Caspase 3
  • Caspases