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2016 Fiscal Year Final Research Report

Re-expression of Sall1 in podocytes protects against adriamycin-induced nephrosis

Research Project

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Project/Area Number 26860648
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Kidney internal medicine
Research InstitutionJuntendo University

Principal Investigator

Yoshiko Hosoe-Nagai  順天堂大学, 医学部, 非常勤助教 (30722764)

Project Period (FY) 2014-04-01 – 2017-03-31
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
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.

Free Research Field

糸球体腎炎

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Published: 2018-03-22  

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