The role of fibrocytes in progressive renal fibrosis

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  • Sakai Norihik
    Disease Control and Homeostasis, Graduate School of Medical Science, Kanazawa University
  • Wada Takashi
    Department of Laboratory Medicine, Graduate School of Medical Science, Kanazawa University
  • Matsushima Kouji
    Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo
  • Kaneko Shuichi
    Disease Control and Homeostasis, Graduate School of Medical Science, Kanazawa University

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Fibrosis is a common pathway resulting in organ failure. Renal fibrosis is a progressive and potentially lethal disease caused by diverse clinical entities. The degree of renal fibrosis well correlates with the prognosis of renal diseases independent of their etiologies. Fibrocytes are peculiar circulating cells that share markers of leukocytes as well as mesenchymal cells. A considerable number of fibrocytes dual positive for CD45 and type I collagen or CD34 and type I collagen infiltrated the interstitium along with the progression of fibrosis in an experimental murine renal fibrosis model. Most fibrocytes in the kidneys were positive for CCR7. In addition, a ligand for CCR7, secondary lymphoid tissue chemokine (SLC/CCL21) co-localized with high endothelial venule-like vessels in fibrotic kidneys. CCL21/CCR7 blockade reduced the number of infiltrating fibrocytes as well as the extent of renal fibrosis, which was confirmed by a decrease in renal transcripts of pro α1 chain of type I collagen and transforming growth factor-β1. These findings suggest that CCL21/CCR7 signaling contributes to the progressive renal fibrosis through the regulation of fibrocytes.

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