Scavenger receptor expressions in the kidneys of mice with lipoprotein glomerulopathy
Related Experiment Video
Updated: May 27, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Yoshiro Miyahara1, Shinsuke Nishimura, Maho Watanabe
1Division of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonann-ku, Fukuoka, 814-0180, Japan.
Background:
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).
Method:
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 6 months 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.
Results:
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.
Conclusion:
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.
