scholarly journals The role of Pax2 in mouse prostate development

The Prostate ◽  
2011 ◽  
Vol 72 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Ben Xu ◽  
Arun Hariharan ◽  
Sabita Rakshit ◽  
Gregory R. Dressler ◽  
Deneen M. Wellik
Keyword(s):  
Prostate Development ◽  
Mouse Prostate

scholarly journals The role of the androgen receptor in prostate development and benign prostatic hyperplasia: A review

2020 ◽  
Vol 7 (3) ◽  
pp. 191-202 ◽  
Author(s):  
Renee E. Vickman ◽  
Omar E. Franco ◽  
Daniel C. Moline ◽  
Donald J. Vander Griend ◽  
Praveen Thumbikat ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia ◽  
Prostate Development

Role of GM-CSF in a mouse model of experimental autoimmune prostatitis

2019 ◽  
Vol 317 (1) ◽  
pp. F23-F29 ◽  
Author(s):  
Yaxiao Liu ◽  
Yan Li ◽  
Qinggang Liu ◽  
Zonglong Wu ◽  
Jianfeng Cui ◽  
...  
Keyword(s):  
Mouse Model ◽  
Dorsal Root Ganglia ◽  
Knockout Mice ◽  
Dorsal Root ◽  
Prostate Tissue ◽  
Mrna Levels ◽  
Gm Csf ◽  
Mouse Prostate ◽  
Experimental Autoimmune

The etiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is still unknown. Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to play an important role in the development of autoimmune and inflammatory diseases. Here, we investigated the expression and function of GM-CSF in patients with CP/CPPS and in a mouse model of experimental autoimmune prostatitis (EAP). GM-CSF mRNA levels were detected in expressed prostatic secretions samples from patients with CP/CPPS and in prostate tissue from a mouse model of EAP. The expression of GM-CSF receptor in mouse prostate and dorsal root ganglia were determined using PCR and immunohistochemistry. Behavioral testing and inflammation scoring were performed to evaluate the role of GM-CSF in disease development and symptom severity of EAP using GM-CSF knockout mice. mRNA levels of putative nociceptive and inflammatory markers were measured in the prostate after the induction of EAP. Elevated GM-CSF mRNA levels were observed in expressed prostatic secretions samples from patients with CP/CPPS compared with healthy volunteers. GM-CSF mRNA was also significantly increased in prostate tissue of the EAP mice model. The expression of GM-CSF receptors was confirmed in mouse prostate and dorsal root ganglia. GM-CSF knockout mice showed fewer Infiltrating leukocytes and pain symptoms after the induction of EAP. Deletion of GM-CSF significantly diminished EAP-induced increases of chemokine (C-C motif) ligand 2, chemokine (C-C motif) ligand 3, and nerve growth factor mRNA expression. The results indicated that GM-CSF plays a functional role in the pathogenesis of EAP. GM-CSF may function as a signaling mediator for both inflammation and pain transduction in CP/CPPS.

scholarly journals Wnt Inhibitory Factor 1 (Wif1) Is Regulated by Androgens and Enhances Androgen-Dependent Prostate Development

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6091-6103 ◽  
Author(s):  
Kimberly P. Keil ◽  
Vatsal Mehta ◽  
Amanda M. Branam ◽  
Lisa L. Abler ◽  
Rita A. Buresh-Stiemke ◽  
...  
Keyword(s):  
Branching Morphogenesis ◽  
Inhibitory Factor ◽  
Urogenital Sinus ◽  
Sexually Dimorphic ◽  
Bud Formation ◽  
Prostate Development ◽  
Mouse Prostate ◽  
Necessary And Sufficient ◽  
Wnt Inhibitory Factor 1 ◽  
Inhibitory Factor 1

Abstract Fetal prostate development from urogenital sinus (UGS) epithelium requires androgen receptor (AR) activation in UGS mesenchyme (UGM). Despite growing awareness of sexually dimorphic gene expression in the UGS, we are still limited in our knowledge of androgen-responsive genes in UGM that initiate prostate ductal development. We found that WNT inhibitory factor 1 (Wif1) mRNA is more abundant in male vs. female mouse UGM in which its expression temporally and spatially overlaps androgen-responsive steroid 5α-reductase 2 (Srd5a2). Wif1 mRNA is also present in prostatic buds during their elongation and branching morphogenesis. Androgens are necessary and sufficient for Wif1 expression in mouse UGS explant mesenchyme, and testicular androgens remain necessary for normal Wif1 expression in adult mouse prostate stroma. WIF1 contributes functionally to prostatic bud formation. In the presence of androgens, exogenous WIF1 protein increases prostatic bud number and UGS basal epithelial cell proliferation without noticeably altering the pattern of WNT/β-catenin-responsive Axin2 or lymphoid enhancer binding factor 1 (Lef1) mRNA. Wif1 mutant male UGSs exhibit increased (Sfrp)2 and (Sfrp)3 expression and form the same number of prostatic buds as the wild-type control males. Collectively our results reveal Wif1 as one of the few known androgen-responsive genes in the fetal mouse UGM and support the hypothesis that androgen-dependent Wif1 expression is linked to the mechanism of androgen-induced prostatic bud formation.

scholarly journals In Utero Exposure to TCDD Alters Wnt Signaling During Mouse Prostate Development: Linking Ventral Prostate Agenesis to Downregulated β-Catenin Signaling

2014 ◽  
Vol 141 (1) ◽  
pp. 176-187 ◽  
Author(s):  
Andrew J. Schneider ◽  
Robert W. Moore ◽  
Amanda M. Branam ◽  
Lisa L. Abler ◽  
Kimberly P. Keil ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
In Utero ◽  
Ventral Prostate ◽  
In Utero Exposure ◽  
Prostate Development ◽  
Mouse Prostate

scholarly journals Androgen action in cell fate and communication during prostate development at single-cell resolution

Development ◽  
2020 ◽  
pp. dev.196048
Author(s):  
Dong-Hoon Lee ◽  
Adam W. Olson ◽  
Jinhui Wang ◽  
Won Kyung Kim ◽  
Jiaqi Mi ◽  
...  
Keyword(s):  
Single Cell ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Molecular Mechanisms ◽  
Bud Formation ◽  
Master Regulators ◽  
Prostate Development ◽  
Dynamic Cell ◽  
Cell Signaling Networks

Androgens/androgen receptor (AR) mediated signaling pathways are essential for prostate development, morphogenesis, and regeneration. Specifically, stromal AR-signaling has been shown to be essential for prostatic initiation. However, the molecular mechanisms underlying AR-initiated mesenchymal-epithelial interactions in prostate development remain unclear. Here, using a newly generated mouse model, we directly addressed the fate and role of genetically marked AR-expressing cells during embryonic prostate development. Androgen signaling-initiated signaling pathways were identified in mesenchymal niche populations at single cell transcriptomic resolution. The dynamic cell-signaling networks regulated by stromal AR were characterized in regulating prostatic epithelial bud formation. Pseudotime analyses further revealed the differentiation trajectory and fate of AR-expressing cells in both prostatic mesenchymal and epithelial cell populations. Specifically, the cellular properties of Zeb1-expressing progenitors were assessed. Selective deletion of AR signaling in a subpopulation mesenchymal rather than epithelial cells dysregulates the expression of the master regulators and significantly impairs prostatic bud formation. These data provide novel, high-resolution evidence demonstrating the important role of mesenchymal androgen signaling as cellular niches controlling prostate early development by initiating dynamic mesenchyme-epithelia cell interactions.

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