Talk:Prostate Development

2009

The role of Wnt5a in prostate gland development

Dev Biol. 2009 Apr 15;328(2):188-99. Epub 2009 Jan 14.

Huang L, Pu Y, Hu WY, Birch L, Luccio-Camelo D, Yamaguchi T, Prins GS.

Department of Urology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60614, USA.

Abstract

The Wnt genes encode a large family of secreted glycoproteins that play important roles in controlling tissue patterning, cell fate and proliferation during development. Currently, little is known regarding the role(s) of Wnt genes during prostate gland development. The present study examines the role of the noncanonical Wnt5a during prostate gland development in rat and murine models. In the rat prostate, Wnt5a mRNA is expressed by distal mesenchyme during the budding stage and localizes to periductal mesenchymal cells with an increasing proximal-to-distal gradient during branching morphogenesis. Wnt5a protein is secreted and localizes to periductal stroma, extracellular matrix and epithelial cells in the distal ducts. While Wnt5a expression is high during active morphogenesis in all prostate lobes, ventral prostate (VP) expression declines rapidly following morphogenesis while dorsal (DP) and lateral lobe (LP) expression remains high into adulthood. Steroids modulate prostatic Wnt5a expression during early development with testosterone suppressing Wnt5a and neonatal estrogen increasing expression. In vivo and ex vivo analyses of developing mouse and rat prostates were used to assess the functional roles of Wnt5a. Wnt5a(-/-) murine prostates rescued by organ culture exhibit disturbances in bud position and directed outgrowth leading to large bulbous sacs in place of elongating ducts. In contrast, epithelial cell proliferation, ductal elongation and branchpoint formation are suppressed in newborn rat prostates cultured with exogenous Wnt5a protein. While renal grafts of Wnt5a(-/-) murine prostates revealed that Wnt5a is not essential for cyto- and functional differentiation, a role in luminal cell polarity and lumenization of the ducts was indicated. Wnt5a suppresses prostatic Shh expression while Shh stimulates Wnt5a expression in a lobe-specific manner during early development indicating that Wnt5a participates in cross-talk with other members of the gene regulatory network that control prostate development. Although Wnt5a does not influence prostatic expression of other Wnt morphogens, it suppresses Wif-1 expression and can thus indirectly modulate Wnt signaling. In summary, the present finds demonstrate that Wnt5a is essential for normal prostate development where it regulates bud outgrowth, ductal elongation, branching, cell polarity and lumenization. These findings contribute to the growing body of knowledge on regulatory mechanisms involved in prostate gland development which are key to understanding abnormal growth processes associated with aging.

PMID: 19389372 PMCID: PMC2828764

http://www.ncbi.nlm.nih.gov/pubmed/19389372

Imaging of the seminal vesicle and vas deferens

Radiographics. 2009 Jul-Aug;29(4):1105-21.

Kim B, Kawashima A, Ryu JA, Takahashi N, Hartman RP, King BF Jr.

Department of Radiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA. kim.bohyun@mayo.edu Abstract The seminal vesicle (SV) and vas deferens (VD) are ancillary but essential urogenital organs. Understanding their embryologic features and anatomy can be helpful in evaluating various disorders of these organs. Recently, cross-sectional imaging modalities, including ultrasonography, computed tomography, and magnetic resonance (MR) imaging, have been increasingly used for evaluation of the SV and VD. The development of these organs is closely related to that of urinary organs, including the kidneys and ureters. Frequently, unilateral SV agenesis is associated with renal agenesis, and bilateral SV or VD agenesis is associated with mutations of the cystic fibrosis gene. Congenital SV cysts are commonly associated with ipsilateral renal agenesis or dysgenesis. These congenital anomalies can be well evaluated with MR imaging. Inflammation, post-radiation therapy changes, and amyloidosis of the SV appear as diffuse wall thickening and may mimic tumor invasion by prostate cancer. Primary neoplasms involving the SV and VD are extremely rare, whereas secondary neoplasms are much more common. Carcinoma from the prostate, bladder, or rectum can directly invade the SV and VD. Typical MR imaging findings of such invasion include a low-signal-intensity mass on T2-weighted images or soft-tissue thickening in the SV or VD along with loss of normal architecture.

Copyright RSNA, 2009

PMID: 19605659 http://www.ncbi.nlm.nih.gov/pubmed/19605659 http://radiographics.rsna.org/content/29/4/1105.long

2003

Quantification of expression of netrins, slits and their receptors in human prostate tumors

Int J Cancer. 2003 Jan 20;103(3):306-15. Latil A, Chêne L, Cochant-Priollet B, Mangin P, Fournier G, Berthon P, Cussenot O.

UroGene, Génopole, Evry Cedex, France. a.latil@urogene.com

Abstract

Recently, DCC (Deleted in Colorectal Cancer) protein has been forwarded as a receptor for netrin. The Netrin/DCC complex is critical for axon guidance and cell migration. In the developing nervous system, netrin protein secreted by midline cells attracts commissural axons by activating the DCC receptor on growth cones. This attraction can be switched to repulsion or silenced completely, depending on the DCC binding partner. The potential suppressor function of DCC in prostate tumorigenesis, through a still unknown mechanism, prompted us to quantify the expression of several genes involved in this axon guidance pathway. The relative expression levels of DCC, NEO1, NTN1, NTN2L, NTN4, UNC5C, Slit1, Slit2, Slit3, Robo1 and Robo2 were simultaneous quantified in 48 tumors and 7 normal prostate tissues by using real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). A reduction in DCC, NEO1, NTN1 and NTN4 expression was observed in prostate tumors, while many of the same prostate tumors over-expressed either Slit genes or their receptors, Robo.

Copyright 2002 Wiley-Liss, Inc. PMID: 12471613