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Identifying genomic pathways associated with fibrosis in diabetic nephropathy
Summary Data Summary
Investigator Bomsztyk, Karol
Description Diabetic nephropathy (DN) is the most common cause of end-stage renal disease in
the US. Our long term goal is to define mechanisms responsible for progression
and reversal of DN, and to establish a basis for therapeutics to reverse DN.
Fibrosis in the glomerulus and tubulointerstitium is a major contributor to the
decline of renal function in DN. Although traditionally fibrosis in DN has been
thought to be irreversible there are indications that resolution of renal
fibrotic lesions is possible. Importantly there is evidence that regression of
fibrosis is sufficient to improve renal function. Still, there are no treatments
specifically indicated to target reversal of renal fibrosis. BTBR mouse strain
with the ob/ob leptin-deficiency mutation develops Type 2 diabetes (T2D) and
severe DN. There is evidence that full reversibility of DN can be achieved in
this model with leptin replacement. We have developed a high-throughput
multiplex chromatin immunoprecipitation platform, Matrix ChIP-MeDIP, and
computational tools that taken together for the first time make it possible to
simultaneously study epigenetic events as well as nuclear signaling cascades
immediately upstream of chromatin and transcriptional events. The Specific Aim
of this pilot project is to demonstrate the feasibility of defining differences
in epigenetic changes at fibrogenesis-related genes in kidneys from wild-type
BTBR compared to the T2D BTBR ob/ob mice.
Status In Progress
Public Release 10/28/2013
Data Collected? Data will not be collected for this catalog item
Species M. musculus
Animal Age Measured In: week(s) post-natal (w)
Data Analysis
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Phenotype Measurements00
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Histology Images00
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Documents11

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