Suppr超能文献

肌营养不良蛋白聚糖对于维持小鼠前列腺管腔上皮基底膜或细胞极性不是必需的。

Dystroglycan is not required for maintenance of the luminal epithelial basement membrane or cell polarity in the mouse prostate.

机构信息

Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, Iowa, USA.

出版信息

Prostate. 2010 May 15;70(7):777-87. doi: 10.1002/pros.21110.

Abstract

BACKGROUND

Dystroglycan is a cell-surface receptor for extracellular matrix proteins including laminins and perlecan. Prior studies have shown its involvement in assembly and/or maintenance of basement membrane structures, cell polarity and tissue morphogenesis; and its expression is often reduced in prostate and other cancers. However, the role of dystroglycan in normal epithelial tissues such as the prostate is unclear.

METHODS

To investigate this, we disrupted dystroglycan expression in the prostate via a conditional gene targeting strategy utilizing Cre recombinase expressed in luminal prostate epithelial cells.

RESULTS

Contrary to expectations, deletion of dystroglycan in luminal epithelial cells resulted in no discernable phenotype as judged by histology, basement membrane ultrastructure, localization of dystroglycan ligands, cell polarity or regenerative capacity of the prostate following castration. Dystroglycan expression remains in keratin-5-positive basal cells located in the proximal ducts where dystroglycan expression is elevated in regenerating prostates.

CONCLUSIONS

Our results show that dystroglycan in luminal epithelial cells is not required for the maintenance of basement membranes, cell polarity or prostate regeneration. However, it is possible that persistent dystroglycan expression in the basal cell compartment may support these or other functions.

摘要

背景

层粘连蛋白和 Perlecan 等细胞外基质蛋白的细胞表面受体是 dystroglycan。先前的研究表明它参与了基底膜结构、细胞极性和组织形态发生的组装和/或维持;其表达在前列腺癌和其他癌症中常常降低。然而,dystroglycan 在前列腺等正常上皮组织中的作用尚不清楚。

方法

为了研究这一点,我们利用在腔上皮细胞中表达的 Cre 重组酶,通过条件性基因靶向策略破坏前列腺中的 dystroglycan 表达。

结果

出乎意料的是,腔上皮细胞中 dystroglycan 的缺失并没有导致组织学、基底膜超微结构、dystroglycan 配体的定位、细胞极性或去势后前列腺的再生能力的可察觉表型。dystroglycan 的表达仍然存在于位于近端导管中的角蛋白 5 阳性基底细胞中,在再生的前列腺中,dystroglycan 的表达升高。

结论

我们的结果表明,腔上皮细胞中的 dystroglycan 对于维持基底膜、细胞极性或前列腺再生不是必需的。然而,基底细胞隔室中持续的 dystroglycan 表达可能支持这些或其他功能。

相似文献

3
Distribution of dystroglycan in normal adult mouse tissues.
J Histochem Cytochem. 1998 Apr;46(4):449-57. doi: 10.1177/002215549804600404.
4
Integrin and dystroglycan compensate each other to mediate laminin-dependent basement membrane assembly and epiblast polarization.
Matrix Biol. 2017 Jan;57-58:272-284. doi: 10.1016/j.matbio.2016.07.005. Epub 2016 Jul 20.
7
The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.
Biomaterials. 2019 Oct;218:119337. doi: 10.1016/j.biomaterials.2019.119337. Epub 2019 Jul 9.
9
Reduced expression of dystroglycan in breast and prostate cancer.
Hum Pathol. 2001 Aug;32(8):791-5. doi: 10.1053/hupa.2001.26468.
10
Intracellular polarity protein PAR-1 regulates extracellular laminin assembly by regulating the dystroglycan complex.
Genes Cells. 2009 Jul;14(7):835-50. doi: 10.1111/j.1365-2443.2009.01315.x. Epub 2009 Jun 22.

引用本文的文献

1
Involvement of abnormal dystroglycan expression and matriglycan levels in cancer pathogenesis.
Cancer Cell Int. 2022 Dec 9;22(1):395. doi: 10.1186/s12935-022-02812-7.
2
The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.
Biomaterials. 2019 Oct;218:119337. doi: 10.1016/j.biomaterials.2019.119337. Epub 2019 Jul 9.
3
Integrins and epithelial cell polarity.
J Cell Sci. 2014 Aug 1;127(Pt 15):3217-25. doi: 10.1242/jcs.146142. Epub 2014 Jul 2.
4
Loss of LARGE2 disrupts functional glycosylation of α-dystroglycan in prostate cancer.
J Biol Chem. 2013 Jan 25;288(4):2132-42. doi: 10.1074/jbc.M112.432807. Epub 2012 Dec 6.
5
Slow disease progression in a C57BL/6 pten-deficient mouse model of prostate cancer.
Am J Pathol. 2011 Jul;179(1):502-12. doi: 10.1016/j.ajpath.2011.03.014. Epub 2011 May 7.
6
Dystroglycan controls signaling of multiple hormones through modulation of STAT5 activity.
J Cell Sci. 2010 Nov 1;123(Pt 21):3683-92. doi: 10.1242/jcs.070680. Epub 2010 Oct 12.

本文引用的文献

1
A luminal epithelial stem cell that is a cell of origin for prostate cancer.
Nature. 2009 Sep 24;461(7263):495-500. doi: 10.1038/nature08361. Epub 2009 Sep 9.
4
Laminin alpha 5 influences the architecture of the mouse small intestine mucosa.
J Cell Sci. 2008 Aug 1;121(Pt 15):2493-502. doi: 10.1242/jcs.025528. Epub 2008 Jul 15.
6
Dystroglycan loss disrupts polarity and beta-casein induction in mammary epithelial cells by perturbing laminin anchoring.
J Cell Sci. 2006 Oct 1;119(Pt 19):4047-58. doi: 10.1242/jcs.03103. Epub 2006 Sep 12.
8
Proximal prostatic stem cells are programmed to regenerate a proximal-distal ductal axis.
Stem Cells. 2006 Aug;24(8):1859-68. doi: 10.1634/stemcells.2005-0585. Epub 2006 Apr 27.
9
C. elegans dystroglycan DGN-1 functions in epithelia and neurons, but not muscle, and independently of dystrophin.
Development. 2006 May;133(10):1911-21. doi: 10.1242/dev.02363. Epub 2006 Apr 12.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验