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BASP1 promotes apoptosis in diabetic nephropathy
Maria Dolores Sanchez-Niño1, Ana Belen Sanz, Corina Lorz
1Nefrología, Fundación Jiménez Díaz, Universidad Autonoma de Madrid and Instituto Reina Sofia de Investigaciones Nefrológicas-IRSIN, Madrid, Spain.
Journal of the American Society of Nephrology : JASN
|January 30, 2010
Summary
Researchers identified BASP1 as a key factor causing cell death in diabetic nephropathy (DN). Lowering BASP1 levels protected kidney cells, suggesting it
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Apoptosis plays a role in diabetic nephropathy (DN) pathogenesis.
- The precise mechanisms of diabetes-induced kidney cell death remain unclear.
Purpose of the Study:
- To identify novel genes involved in diabetes-induced apoptosis in the kidney.
- To investigate the role of BASP1 in diabetic nephropathy.
Main Methods:
- Functional genomics screen to identify apoptosis-inducing cDNAs.
- Transcriptional profiling of human DN renal biopsies.
- In vitro studies using human tubular epithelial cells.
- siRNA-mediated knockdown of BASP1.
Main Results:
- BASP1 was identified as a proapoptotic factor upregulated in DN.
- High glucose and inflammatory conditions increased BASP1 expression in tubular cells.
- BASP1 overexpression induced apoptosis; BASP1 knockdown conferred protection.
- Renal BASP1 was also upregulated in hypertensive models.
Conclusions:
- BASP1 is a key proapoptotic factor in diabetic nephropathy.
- BASP1 may also be implicated in hypertensive nephropathy.
- Targeting BASP1 could offer a therapeutic strategy for kidney diseases.
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