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Diabetes and miRNA
Summary Data Summary
Applicant Bornfeldt, Karin
E-Mail Address bornf@u.washington.edu
Project Title Diabetes and miRNA
CBU ID 13GHSU308
External SubContract ID 25034-33
Diabetic Complication Cardiovascular
Funding Program Group Pilot & Feasibility [PF2013]
Abstract Diabetes mellitus is associated with a number of devastating long-term
complications, the most important in terms of increased mortality being
macrovascular complications (atherosclerosis) leading to cardiovascular disease.
In mouse models of diabetes-accelerated atherosclerosis, accumulation of
macrophages in the blood vessel wall is due to a diabetes-induced inflammatory
activation of these cells, and blocking this inflammatory activation completely
prevents diabetes-accelerated atherosclerosis. We are therefore in the process
of identifying intracellular mediators of this diabetes-induced macrophage
inflammatory activation, with the hope of finding new drug targets to treat or
prevent diabetes-accelerated atherosclerosis and perhaps other complications of
diabetes that are dependent on macrophage activation. To this end, we have
started to investigate the role of microRNAs in mediating diabetes-induced
macrophage activation. Preliminary results demonstrate that diabetes causes
marked suppression of microRNA-486-5p in macrophages. The best characterized and
validated targets of microRNA-486 (miR-486) are Phosphatase and tensin homolog
(PTEN; an inhibitor of PI3-kinase action) and Forkhead box protein O1 (FoxO1; a
transcription factor downstream of PI3-kinase which promotes inflammation). The
goal of this P&F project is to evaluate whether miR-486 is a mediator of
diabetes-induced macrophage inflammatory activation. We propose to address two
questions: 1). Is miR-486 suppressed by diabetes in monocytes and macrophages
and is this associated with hyperglycemia and suppression of Ank1 expression?;
and 2). Is downregulation of miR-486 in macrophages sufficient for inflammatory
activation, mimicking the effect of diabetes? Our long-term goal is to identify
new drug targets to deactivate monocytes and macrophages and prevent
atherosclerosis and other diabetes complications.
Application PDF Application Research Plan
Status Contract Executed
Key Personnel
Salary Total Costs 29960
Supply Total Costs 11000
Equipment Total Costs 0
Travel/Other Total Costs 5965
Direct Costs 46925
Indirect Costs Proposed 34725
Total Costs Proposed 81650
Total Costs Approved 81650
Start Date 10/1/2013
End Date 9/30/2014
IFO Name Arias, Lynette
IFO E-Mail Address osp@u.washington.edu
IACUC/IRB No. A3464-01
IACUC/IRB Institution University of Washington
Entity ID No. 91-6001537
Report Request Date 10/30/2014
T1D NO
TypeCount
Invoices 11
Progress Reports 1
Data Submission


Invoices
UrlCBU IDExternal IDInstitutionDateDirectIndirectInvoiceBalancePDF
  View  13GHSU30825034-33University of Washington9/10/2014$17,089.72-$17,089.72$95.13View PDF
  View  13GHSU30825034-33University of Washington8/8/2014$15,994.37-$15,994.37$95.13View PDF
  View  13GHSU30825034-33University of Washington7/9/2014$12,455.11-$12,455.11$95.13View PDF
  View  13GHSU30825034-33University of Washington6/11/2014$2,608.87-$2,608.87$95.13View PDF
  View  13GHSU30825034-33University of Washington5/9/2014$4,135.47-$4,135.47$95.13View PDF
  View  13GHSU30825034-33University of Washington4/10/2014$3,189.93-$3,189.93$95.13View PDF
  View  13GHSU30825034-33University of Washington3/11/2014$2,750.59$2,035.44$4,786.03$95.13View PDF
  View  13GHSU30825034-33University of Washington2/11/2014$2,288.53$1,693.51$3,982.04$95.13View PDF
  View  13GHSU30825034-33University of Washington11/25/2014$55.11-$55.11$95.13View PDF
  View  13GHSU30825034-33University of Washington10/10/2014$12,969.74-$12,969.74$95.13View PDF
  View  13GHSU30825034-33University of Washington1/9/2014$2,464.64$1,823.84$4,288.48$95.13View PDF
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