Sall1, an Indispensable Protein for Kidney Development, Plays a Renoprotective Role in Podocyte Injury

抄録

Objective: Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis and known as the initial key step for matenephros development. Sall1-deficient animals die at birth due to kidney deficits. However, its function in mature podocytes and/or injured podocytes has not been characterized. The present study indicated the role of Sall1 in mature podocytes as well as in injured podocytes.
Materials and Methods: To clarify the role of Sall1 in mature podocytes, we generated podocyte-specific Sall1 KO (pSall1 KO) mice. To clarify the role of Sall1 in injured podocytes, we used Lipopolysaccharide (LPS) -injected mice as a minimal-change disease (MCD) model and ADR-injected mice as a nephrosis and glomerulosclerosis model.
Results: We observed that the pSall1 KO mice showed no obvious phenotype under physiological conditions. There was no significant difference in the level of urinary protein among WT mice and pSall1 KO mice groups 48 hours after the injection of LPS. The level of urinary protein was significantly increased in pSall1 KO mice on day 28 after ADR injection. Sall1 affected the localization of the slit diaphragm protein nephrin in ADR-injected pSall1 KO mice.
Conclusions: Sall1 may have a crucial renoprotective role in the mechanism of recovery from severe podocyte injury.