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有梗阻和无梗阻的多囊性发育不良肾的免疫组织化学对比研究

Comparative immunohistochemical study of multicystic dysplastic kidneys with and without obstruction.

作者信息

Rojas Claudia P, Urbiztondo Arnel K, Bruce Jocelyn H, Rodriguez Maria M

机构信息

Department of Pathology, University of Miami, Holtz's Children's Hospital, Miami, Florida 33136, USA.

出版信息

Fetal Pediatr Pathol. 2011;30(4):209-19. doi: 10.3109/15513815.2011.572960. Epub 2011 Jun 20.

DOI:10.3109/15513815.2011.572960
PMID:21689023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3156438/
Abstract

Etiology of multicystic dysplastic kidney (MCDK) remains unknown. Not all cases are associated with obstruction. We compared by immunohistochemistry 17 cases of MCDK (10 cases with and seven without obstruction) to 17 controls and 20 fetal kidneys. TGF-β was negative in obstructive MCDKs and positive in nonobstructive MCDK. IGF2 was overexpressed in obstructive and underexpressed in nonobstructive MCDKs. PAX2, BCL-2, and β-catenin were expressed equally in obstructive and nonobstructive dysplasia. TGF-β and IGF2 work by different mechanisms in obstructive and nonobstructive MCDKs, but there are no differences among PAX 2, BCL-2, and β-catenin in obstructive versus nonobstructive dysplasia.

摘要

多囊性发育不良肾（MCDK）的病因尚不清楚。并非所有病例都与梗阻有关。我们通过免疫组织化学方法，将17例MCDK（10例有梗阻，7例无梗阻）与17例对照及20例胎儿肾脏进行了比较。转化生长因子-β（TGF-β）在梗阻性MCDK中呈阴性，在非梗阻性MCDK中呈阳性。胰岛素样生长因子2（IGF2）在梗阻性MCDK中过度表达，在非梗阻性MCDK中表达不足。配对盒基因2（PAX2）、B细胞淋巴瘤-2（BCL-2）和β-连环蛋白在梗阻性和非梗阻性发育不良中表达相同。TGF-β和IGF2在梗阻性和非梗阻性MCDK中通过不同机制起作用，但在梗阻性与非梗阻性发育不良中，PAX2、BCL-2和β-连环蛋白之间没有差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0422/3156438/c3b79ceae97a/updp30-209-f1.jpg

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本文引用的文献

1
Loss of nephrocystin-3 function can cause embryonic lethality, Meckel-Gruber-like syndrome, situs inversus, and renal-hepatic-pancreatic dysplasia.
Am J Hum Genet. 2008 Apr;82(4):959-70. doi: 10.1016/j.ajhg.2008.02.017. Epub 2008 Mar 27.
2
Canonical WNT/beta-catenin signaling is required for ureteric branching.
Dev Biol. 2008 May 1;317(1):83-94. doi: 10.1016/j.ydbio.2008.02.010. Epub 2008 Feb 21.
3
The stumpy gene is required for mammalian ciliogenesis.
Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):2853-8. doi: 10.1073/pnas.0712385105. Epub 2008 Feb 19.
4
Epidermal growth factor and transforming growth factor-beta1 enhance HK-2 cell migration through a synergistic increase of matrix metalloproteinase and sustained activation of ERK signaling pathway.
Exp Cell Res. 2007 Jul 1;313(11):2367-77. doi: 10.1016/j.yexcr.2007.03.022. Epub 2007 Mar 30.
5
Smad1, beta-catenin and Tcf4 associate in a molecular complex with the Myc promoter in dysplastic renal tissue and cooperate to control Myc transcription.
Development. 2005 Jan;132(1):215-25. doi: 10.1242/dev.01573. Epub 2004 Dec 2.
6
Potential biological role of transforming growth factor-beta1 in human congenital kidney malformations.
Am J Pathol. 2000 Nov;157(5):1633-47. doi: 10.1016/s0002-9440(10)64801-8.
7
Decreased bcl-2 expression in segmental renal dysplasia suggests a role in its morphogenesis.
Br J Urol. 1997 Jul;80(1):140-4. doi: 10.1046/j.1464-410x.1997.00235.x.
8
Insulin-like growth factor (IGF) and IGF binding protein gene expression in multicystic renal dysplasia.
J Am Soc Nephrol. 1997 Jan;8(1):85-94. doi: 10.1681/ASN.V8185.
9
Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse.
Am J Physiol. 1996 Jul;271(1 Pt 2):F184-93. doi: 10.1152/ajprenal.1996.271.1.F184.
10
The PAX2 tanscription factor is expressed in cystic and hyperproliferative dysplastic epithelia in human kidney malformations.
J Clin Invest. 1996 Jul 15;98(2):451-9. doi: 10.1172/JCI118811.

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