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Protection by metallothionein from a...

Yang, Lu.

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Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy./
Author:	Yang, Lu.
Description:	38 p.
Notes:	Adviser: Paul N. Epstein.
Contained By:	Masters Abstracts International46-02.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1448599
ISBN:	9780549251187

Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy.
Yang, Lu.

Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy. - 38 p.

Adviser: Paul N. Epstein.

Thesis (M.S.)--University of Louisville, 2007.

This thesis is divided into two different parts. Part one is about metallothionein protection from Adriamycin induced nephropathy. Part two is the proposal of gene expression during progression of diabetic nephropathy.

ISBN: 9780549251187Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy.
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020 $a 9780549251187
035 $a (UMI)AAI1448599
035 $a AAI1448599
040 $a UMI $c UMI
100 1 $a Yang, Lu. $3 1070654
245 1 0 $a Protection by metallothionein from adriamycin induced nephropathy in mice and gene expression profiling during progression of diabetic nephropathy.
300 $a 38 p.
500 $a Adviser: Paul N. Epstein.
500 $a Source: Masters Abstracts International, Volume: 46-02, page: 0941.
502 $a Thesis (M.S.)--University of Louisville, 2007.
520 $a This thesis is divided into two different parts. Part one is about metallothionein protection from Adriamycin induced nephropathy. Part two is the proposal of gene expression during progression of diabetic nephropathy.
520 $a Part I. Adriamycin (ADR) is a well known drug for establishing nephropathy in rodents. In some strains of mice ADR produces proteinuria with additional pathologies including glomerular sclerosis and tubular injury. Though the molecular mechanism of ADR nephrotoxicity is not clear, one hypothesis for ADR induced renal damage is the induction of oxidative stress.
520 $a In this thesis, we used transgenic mice (NMT3), which over-expressed the antioxidant protein metallothionein (MT) in glomerular epithelial cells (podocytes), to study the protective potential of MT on ADR nephropathy. In the experiment, two groups of mice (FVB control and NMT3 transgenic) received 11mg/body weight ADR through tail vein injection at 3 months of age. Twenty-four hour urine were then collected at time points of 5 days, 1 week, 2 weeks and 4 weeks. Four transgenic and four control mice were sacrificed on the 5 th day after ADR injection to obtain kidney tissues for immunohistochemistry, ADR injected mice were compared to untreated FVB and Nmt3 as controls.
520 $a Urine albumin analysis showed that mice excreted significantly more urine albumin after ADR injection. Nmt3 mice showed significant protection from elevated urine albumin excretion. Glomerular histopathology revealed that ADR reduced podocyte number significantly in FVB mice but not in ADR mice. These results show that the antioxidant protein MT can protect he podocyte from ADR toxicity. They also show that protection of the podocyte is sufficient to protect mice from the proteinuria induced by ADR.
520 $a Part II. It is likely that changes in gene expression are associated with the development of chronic diseases, such as diabetic nephropathy. We are examining renal and glomerular changes in gene expression as diabetic nephropathy develops so that we can get an idea of which genes are involved and play a role in development of the disease. Thus far we have found surprisingly low numbers of genes significantly altered by diabetes in the kidney. More detailed analysis of functional subsets may reveal greater changes. The complement protein C3 was markedly elevated by diabetes in all age groups tested. In addition it was highest in the oldest diabetic group with the greatest level of albuminuria. Analysis of laser capture glomerular RNA samples revealed that heat shock proteins were markedly reduced in diabetic samples. This may indicate a vulnerability of diabetic glomeruli to further damage.
590 $a School code: 0110.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 $a University of Louisville. $3 1017614
773 0 $t Masters Abstracts International $g 46-02.
790 $a 0110
790 1 0 $a Epstein, Paul N., $e advisor
791 $a M.S.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1448599