2016 Fiscal Year Final Research Report
Re-expression of Sall1 in podocytes protects against adriamycin-induced nephrosis
| Project/Area Number |
26860648
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | ポドサイト / Sall1 / 糸球体腎炎 / アポトーシス / シナプトポディン / GRP78 |
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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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| Free Research Field |
糸球体腎炎
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