Roles of bone marrow cells in glomerular diseases.
Bone marrow transplantation (BMT) has been used as a tool to investigate various roles of bone marrow cells in glomerular diseases. BMT from IgA nephropathy-prone mice caused glomerular IgA deposition associated with increased circulating macromolecular IgA in normal recipients. Conversely, glomerular mesangial lesions of IgA nephropathy-prone mice were markedly diminished by BMT from normal donors, and the circulating levels of macromolecular IgA were also decreased in the recipients. These data suggest that IgA nephropathy may be a stem-cell disease. BMT clearly decreased the glomerular injuries in glomerular diseases other than murine IgA nephropathy. Theoretically, one mechanism underlying the therapeutic effect of BMT is the replacement of the recipient's destructive immune cells with the donor's bone marrow cells. Interestingly, when BMT was performed by using bone marrow cells of green fluorescent protein (GFP) transgenic mice to investigate the differentiation of bone marrow stem cells in recipients, it was revealed that bone marrow-derived cells differentiated into glomerular cells in mice receiving BMT. This result suggests an alternative mechanism, in that bone marrow cells not only replace harmful immune cells but that they also replenish injured glomerular cells in BMT recipients, which results in the repair of glomerular lesions after BMT. In addition, the glomerular remodeling could participate in maintaining glomerular homeostasis. If the mechanisms of glomerular remodeling are investigated, this could offer a new therapeutic strategy for the repair of glomerular injuries.
Imasawa
Toshiyuki
T
Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School, 1981 Tsujido, Kamoda, Kawagoe, Saitama 350-8550, Japan. imasawa@now.mfnet.ne.jp
D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology / Q000502:physiology*; D016026:Bone Marrow Transplantation; D005922:Glomerulonephritis, IGA / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D006801:Humans