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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Lysophosphatidylserine (LysoPS) is a rather novel lysophospholipids mediator, which exerts several physiological properties, especially in the fields of immune response, through its three GPCRs, GPR34, P2Y10, and GPR174. In this study, we aimed to elucidate the potential roles of LysoPS in the pathogenesis of kidney diseases, using HIGA mice, a murine IgA nephropathy model.
We investigated the modulations of plasma LysoPS levels as well as the renal expression of its receptors in HIGA mice and Balb/c control mice. Then, we administered 28-week-old HIGA mice with 18:1 LysoPS intraperitoneally for ten days and investigated the phenotypes. We also investigated the impacts of the knockout of GPR34 or P2Y10 on the phenotypes of 28-week-old HIGA mice. Lastly, we investigated the underlying mechanisms of the modulations of IgA nephropathy phenotypes using MES-13 cells and HK-2 cells.
[1] In HIGA mice, plasma LysoPS levels began to decrease at 12-week-old, when the IgA phenotypes had not become obvious, and the decline progressed until 32-week-old, when the phenotypes were completed. Among three LysoPS receptors, the renal expression levels of GPR34 and P2Y10 were lower in HIGA mice.
[2] The administration of 18:1 LysoPS improved the histological phenotypes, especially the proliferation of mesangium, as well as urine protein levels. In addition, the renal expression of inflammation and fibrosis-related genes were lower in the HIGA mice treated with LysoPS, whereas the plasma IgA levels remained unchanged.
[3] The knockout of GPR34 deteriorated, while knockout of P2Y10 ameliorated the phenotypes of IgA nephropathy, such as histological mesangial expansion and urine protein levels.
[4] In vitro, 18:1 LysoPS treatment suppressed the proliferation of MES-13, dose dependently. The stable knockdown of GPR34 blurred the response of MES-13 proliferation to 18:1 LysoPS. In HK-2 cells, 18:1 LysoPS suppressed the expression of CXCL-12, which was inhibited by the knockdown of GPR34, whereas 18:0 LysoPS induced it, which was inhibited by the knockdown of P2Y10. CXCL-12 enhanced the migration of neutrophils. Actually, neutrophils invaded the kidneys more in GPR34KO HIGA mice, while less in P2Y10KO HIGA mice.
These results suggested that 18:1 LysoPS might mainly act on GPR34, which suppressed the proliferation of mesangial cells and the expression of CXCL-12, which would ameliorate the phenotypes of HIGA mice, while 18:0 LysoPS might augment the expression of CXCL-12 through the activation of P2Y10, which might deteriorate the phenotypes of HIGA mice. LysoPS might serve as a possible biomarker and therapeutic target for kidney diseases, including IgA nephropathy.
