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Karol Bomsztyk
Personal Information
Title
Professor
Expertise
Nephropathy
Institution
University of Washington
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Type
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Grants/SubContracts
1
Progress Reports
1
Publications
4
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0
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2
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Progress Reports
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Identifying genomic pathways associated with fibrosis in diabetic nephropathy
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. The Alpers lab has shown that the BTBR mouse strain with the ob/ob leptin-deficiency mutation develops Type 2 diabetes (T2D) and severe DN. We present evidence that full reversibility of DN can be achieved in this model with leptin replacement. Several kinase cascades have been implicated in DN (e.g. ERKs, PKCs, Jaks). Chromatin immunoprecipitation (ChIP) assays revealed that kinases/phosphatases/receptors previously implicated in fibrogenesis can be found at genes involved in fibrogenesis. Thus, our overall hypothesis is that characterization of these signaling factors at fibrogenic genes during DN progression and regression can identify new targets for pharmacologic inhibitors to reverse fibrosis in DN. 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 nuclear signaling cascades immediately upstream of chromatin/transcriptional events. The Specific Aim of this pilot project is to demonstrate the feasibility of defining differences in signaling enzymes/receptors at fibrogenesis-related genes in kidneys from wild-type BTBR compared to the T2D BTBR ob/ob mice. The proposed transforming strategy to characterize signaling pathway alterations at fibrogenic genes specific to progression and regression of diabetes complications is the first of its kind to identify and then test novel therapeutic targets in the nucleus for pharmacologic inhibition to prevent and reverse renal fibrosis in DN.
Progress Reports
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Identifying genomic pathways associated with fibrosis in diabetic nephropathy (Bomsztyk, Karol)
10/28/2013
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Submitted By
PubMed ID
Status
Year: 2015; Items: 1
M2 Macrophage Polarization Mediates Anti-inflammatory Effects of Endothelial Nitric Oxide Signaling.
Lee WJ, Tateya S, Cheng AM, Rizzo-DeLeon N, Wang NF, Handa P, Wilson CL, Clowes AW, Sweet IR, Bomsztyk K, Schwartz MW, Kim F
Diabetes
, 2015
Submitted Externally
25845662
Published
Year: 2013; Items: 3
Acyl-CoA synthetase 1 is induced by Gram-negative bacteria and lipopolysaccharide and is required for phospholipid turnover in stimulated macrophages.
Rubinow KB, Wall VZ, Nelson J, Mar D, Bomsztyk K, Askari B, Lai MA, Smith KD, Han MS, Vivekanandan-Giri A, Pennathur S, Albert CJ, Ford DA, Davis RJ, Bornfeldt KE
The Journal of biological chemistry
, 2013 (288), 9957 - 9970
Submitted Externally
23426369
Published
Epigenetic changes in renal genes dysregulated in mouse and rat models of type 1 diabetes.
Komers R, Mar D, Denisenko O, Xu B, Oyama TT, Bomsztyk K
Laboratory investigation; a journal of technical methods and pathology
, 2013 (93), 543 - 552
Bomsztyk, Karol
23508046
Published
Losartan reverses permissive epigenetic changes in renal glomeruli of diabetic db/db mice.
Reddy MA, Sumanth P, Lanting L, Yuan H, Wang M, Mar D, Alpers CE, Bomsztyk K, Natarajan R
Kidney international
, 2013 (85), 362 - 373
Submitted Externally
24088954
Published
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Steering Committee
The DiaComp Steering Committee is the governing body of the consortium. The principle function of this committee is to guide the scientific direction of the consortium. This is accomplished by creating various subcommittees necessary to advance the scientific goals and providing guidance to the broader complications research community. Policies for the consortium are developed through consultation with the
External Evaluation Committee
Nephropathy
The DiaComp Nephropathy Committee has the principal function of furthering the mission of the consortium with regard to diabetic kidney disease.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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