Abstract

To clarify whether dysfunction of the scavenger receptor (SR) participates in the development of lipoprotein glomerulopathy (LPG) in immunoglobulin F(c) receptor γ chain (F(c)Rγ)-deficient mice [F(c)Rγ knock-out (KO) mice] with induced chronic graft-versus-host disease (cGVHD). In wild-type (WT) and F(c)Rγ KO C57BL/6 mice, cGVHD was induced by injection of lymphoid cells from donor Bm12 mice. At 6months after injection, the mice were sacrificed and histologically examined. Total RNA was extracted from the kidneys and cytokine, chemokine, and SR transcript expressions were evaluated by reverse transcription-polymerase chain reaction. Three of 4 female cGVHD(+)/F(c)Rγ KO mice presented LPG in >60% of glomeruli. cGVHD(-) and cGVHD(+)/WT mice did not show LPG. The SRs CD36, CD68, and CXCL16 showed a significant difference in the values of their transcripts between cGVHD(+)/WT and cGVHD(+)/F(c)Rγ KO mice. Among them, only CD36 showed a drastic decline of mRNA expressions in cGVHD(+)/F(c)Rγ KO mice. CD36 may play a crucial role in the development of LPG in F(c)Rγ KO mice with cGVHD. In addition to the apolipoprotein E mutation, dysfunction of lipid clearance in the kidney might be one of the factors for the development of LPG.

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