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PTP1B, a Potential New Therapeutic Target for Diabetic Vascular Complications
Summary Data Summary
Applicant Belin de Chantemele, Eric J
E-Mail Address ebelindechanteme@augusta.edu
Project Title PTP1B, a Potential New Therapeutic Target for Diabetic Vascular Complications
CBU ID 14GHSU1424
External SubContract ID NIDDK00056S3D
Diabetic Complication Cardiovascular
Funding Program Group Pilot & Feasibility [PF2014]
Abstract Endothelial dysfunction is characterized by a reduced nitric oxide (NO)
bioavailability leading to impaired vasodilation and increased inflammation.
Loss of endothelial function is a precursor and major contributor to diabetic
vascular complications, which are the most disabling and life-threatening
complications of diabetes. Despite numerous clinical trials and therapeutic
strategies, preventing and managing endothelial function as well as reducing the
occurrence of cardiovascular events remains a challenge in diabetic patients.
The goal of the present application is to use a novel and clinically relevant
approach consisting of combining the use of human saphenous vein and pulmonary
arteries, with cultured primary endothelial cells, to identify potential new
therapeutic targets for the treatment of diabetic vascular complications.
Preliminary data gathered in human saphenous vein and genetically engineered
mice identified Protein tyrosine phosphatase 1B (PTP1B) and endoplasmic
reticulum (ER) stress as two potential targets. Based on these findings, we
hypothesized that increased PTP1B expression in diabetes causes endothelial
dysfunction by inducing insulin resistance and ER stress, in endothelial cells.
We will test this hypothesis with the two following aims: 1 - To determine
whether diabetes induces a dysfunction of the endothelium secondary to increased
PTP1B expression and ER stress in human saphenous vein and pulmonary artery
endothelial cells, 2 - To determine whether PTP1B deletion or inhibition
protects endothelial cells from diabetes-induced dysfunction by improving
insulin sensitivity, reducing ER stress and increasing eNOS functioning. We
anticipate that these studies will lead to the identification of the molecular
mechanisms by which PTP1B regulates endothelial function. We also expect to
demonstrate that PTP1B is a potential target for the treatment of diabetic
vascular complications.
Application PDF Application Research Plan
Status Contract Executed
Key Personnel
Salary Total Costs 70358
Supply Total Costs 11601
Equipment Total Costs 0
Travel/Other Total Costs 8950
Direct Costs 90909
Indirect Costs Proposed 9091
Total Costs Proposed 100000
Total Costs Approved 100000
Start Date 10/1/2014
End Date 9/30/2015
IFO Name White, Sarah
IFO E-Mail Address ogc@augusta.edu
IACUC/IRB No. 06-04-256
IACUC/IRB Institution Georgia Regents University
Entity ID No. 1-58-1418202-A1
Report Request Date 10/30/2015
T1D NO
TypeCount
Invoices 0
Progress Reports 1
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