| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Sall1 has a crucial role in kidney development. To explore this role in differentiated podocytes, we generated podocyte-specific Sall1-deficient mice (Sall1 KO p/p) and siRNA Sall1 knock down (Sall1 KD) podocytes. Sall1 KO p/p mice showed no proteinuria, however after adriamycin treatment (ADRTx) they showed much of proteinuria and many sclerotic glomeruli. Sall1 KD podocytes showed a loss of synaptopodin following ADRTx. These results indicated that Sall1 has a protective role in podocytes; to explore this mechanism we focused on GRP78. GRP78 expression was higher in ADRTx-Sall1 KO p/p mice than in control mice. Sall1 appeared to influence the expression of GRP78 in injured podocytes. These results suggest that Sall1 is associated with actin re-organization, endoplasmic reticulum stress, and apoptosis in injured podocytes. These protective aspects of Sall1 re-expression in injured podocytes may have the potential to reduce apoptosis and possibly glomerulosclerosis.
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