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The renal microvasculature is highly sensitive to hyperglycemia.
Summary Data Summary
Applicant Ho, Jacqueline
E-Mail Address jacqueline.ho2@chp.edu
Project Title The renal microvasculature is highly sensitive to hyperglycemia.
CBU ID 15GHSU2527
External SubContract ID 25034-77
Diabetic Complication Nephropathy
Funding Program Group Pilot & Feasibility [PF2015]
Abstract The global prevalence of diabetes in pregnancy is increasing, and maternal
hyperglycemia is a significant risk factor for the development of genitourinary
defects and renal malformations. In addition, there is evidence from animal
models that prenatal exposure to hyperglycemia can lead to reduced nephron
endowment, which itself increases the likelihood of chronic kidney disease in
childhood and beyond. Taken together, maternal diabetes represents an important
contributor to the leading cause of chronic kidney disease in children.
Postnatally, the pathogenesis of diabetic nephropathy has been linked to damage
to the microvasculature of the kidney, and aberrant miRNA expression. However,
the molecular mechanisms that underlie the effect of hyperglycemia on kidney
development in utero are unknown.
Our laboratories (Ho and Sims-Lucas) have significant expertise in renal
development, specifically as it pertains to formation of the renal
microvasculature and miRNA function. We have extended the expertise of our
research team by including Dr. Jon Piganelli, a prominent immunologist and
diabetes researcher. We have preliminary data demonstrating that human fetal
kidney endothelial cells undergo oxidative stress when exposed to hyperglycemia.
We hypothesize that maternal hyperglycemia results in impaired nephrogenesis as
a result of altered miRNA function and aberrant differentiation of the kidney
vasculature. Thus, we propose the following:

Aim 1: To characterize the RNA and small RNA transcriptome of human fetal
kidneys and isolated fetal endothelial cells exposed to hyperglycemia.
Aim 2: To validate the mis-regulation of mRNA and miRNA expression in response
to hyperglycemia in vitro and in the streptozotocin-induced mouse model of
diabetes.
Application PDF Application Research Plan
Status Contract Executed
Key Personnel
Salary Total Costs 50407
Supply Total Costs 11527
Equipment Total Costs 0
Travel/Other Total Costs 3000
Direct Costs 64934
Indirect Costs Proposed 35066
Total Costs Proposed 100000
Total Costs Approved 90000
Start Date 10/1/2015
End Date 9/30/2016
IFO Name Woodward, Jennifer
IFO E-Mail Address offres@offres.pitt.edu
IACUC/IRB No. PRO15010510
IACUC/IRB Institution University of Pittsburgh
Entity ID No. 1250965591A6
Report Request Date 10/30/2016
T1D NO
TypeCount
Invoices 7
Progress Reports 1
Data Submission


Invoices
UrlCBU IDExternal IDInstitutionDateDirectIndirectInvoiceBalancePDF
  View  15GHSU252725034-77University of Pittsburgh8/8/2016$521.33$281.52$802.85$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh7/27/2016$7,555.72$4,080.08$11,635.80$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh7/25/2016$16,095.71$2,665.83$18,761.54$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh5/9/2016$8,340.10$4,503.64$12,843.74$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh4/11/2016$11,705.13$5,837.74$17,542.87$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh3/9/2016$15,142.93$7,876.68$23,019.61$11.07View PDF
  View  15GHSU252725034-77University of Pittsburgh10/28/2016$3,495.16$1,887.36$5,382.52$11.07View PDF


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