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2,8-dihydroxyadenine crystal injury ...

Chen, Jianmin.

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2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys./
Author:	Chen, Jianmin.
Description:	152 p.
Notes:	Adviser: Jay A. Tischfield.
Contained By:	Dissertation Abstracts International68-02B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3253035

2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys.
Chen, Jianmin.

2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys. - 152 p.

Adviser: Jay A. Tischfield.

Thesis (Ph.D.)--Rutgers The State University of New Jersey - New Brunswick and University of Medicine and Dentistry of New Jersey, 2007.

Background. APRT-deficient mice develop DHA nephrolithiasis. The two major pathological outcomes in these mice are renal fibrosis and kidney growth retardation. DHA crystal deposition in kidney starts right after birth while the kidney is still developing but the pathology is mild in the first 3 months. This enables us to examine crystal-affected gene expression changes at early stages of stone deposition in developing kidneys and mature kidneys.Subjects--Topical Terms:

1017730
Biology, Genetics.

2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys.
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005 20110523
008 110523s2007 ||||||||||||||||| ||eng d
035 $a (UMI)AAI3253035
035 $a AAI3253035
040 $a UMI $c UMI
100 1 $a Chen, Jianmin. $3 1270452
245 1 0 $a 2,8-dihydroxyadenine crystal injury induces unique gene expression alterations in developing kidneys.
300 $a 152 p.
500 $a Adviser: Jay A. Tischfield.
500 $a Source: Dissertation Abstracts International, Volume: 68-02, Section: B, page: 0737.
502 $a Thesis (Ph.D.)--Rutgers The State University of New Jersey - New Brunswick and University of Medicine and Dentistry of New Jersey, 2007.
520 $a Background. APRT-deficient mice develop DHA nephrolithiasis. The two major pathological outcomes in these mice are renal fibrosis and kidney growth retardation. DHA crystal deposition in kidney starts right after birth while the kidney is still developing but the pathology is mild in the first 3 months. This enables us to examine crystal-affected gene expression changes at early stages of stone deposition in developing kidneys and mature kidneys.
520 $a Experimental design. RNA samples were prepared from kidneys of wild type and APRT-deficient mice of different ages and gender, and were analyzed using the Affymetrix Murine Genome Array U74Av.2. The microarray results for a selected group of genes were validated by real time RT-PCR and by immunohistochemistry.
520 $a Results. (i) gene expression changes caused by APRT deficiency are developmental stage- and gender-dependent; (ii) pro- and anti-inflammatory genes are up-regulated simultaneously in immature APRT-deficient kidneys; (iii) DHA injury promotes epithelial to mesenchymal transition in developing kidneys; (iv) APRT deficiency in developing kidney delays maturation-related gene expression changes; (v) DHA injury in developing kidney increases the expression of a number of stem cell pluripotency markers; (vi) DHA injury induces simultaneous expression of proteins that appear to be critical to kidney development in collecting duct cells of developing kidneys and these cells are quiescent; and (vii) cell injury pathways identified in APRT-deficient mice are relevant to the common calcium oxalate stone disease.
520 $a Conclusions. Our study has for the first time drawn a comprehensive picture of the transcriptional changes caused by chronic injury in developing kidneys. We have identified a list of genes whose expression patterns at least partly explain the developmental stage and gender-specific pathology in APRT-deficient mice. Some of these genes, such as Lcn2, Mcp1 and Mgp, are potential early markers for stone-induced renal injury. Others, such as IL1ra and Socs3 may be drug targets to reduce fibrosis in kidney. Injury-induced quiescence of immature collecting tubule cells, possibly a mechanism to preserve growth potential of these cells, may be responsable for poor kidney differentiation and growth impairment in APRT-deficient mice.
590 $a School code: 0801.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Molecular. $3 1017719
690 $a 0307
690 $a 0369
710 2 $a Rutgers The State University of New Jersey - New Brunswick and University of Medicine and Dentistry of New Jersey. $3 1023857
773 0 $t Dissertation Abstracts International $g 68-02B.
790 $a 0801
790 1 0 $a Tischfield, Jay A., $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3253035