Turco Anne E, Cadena Mark T, Zhang Helen L, Sandhu Jaskiran K, Oakes Steven R, Chathurvedula Thrishna, Peterson Richard E, Keast Janet R, Vezina Chad M
Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, WI, USA.
Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, WI, USA.
Histochem Cell Biol. 2019 Jul;152(1):35-45. doi: 10.1007/s00418-019-01784-6. Epub 2019 Apr 11.
Prostate autonomic and sensory axons control glandular growth, fluid secretion, and smooth muscle contraction and are remodeled during cancer and inflammation. Morphogenetic signaling pathways reawakened during disease progression may drive this axon remodeling. These pathways are linked to proliferative activities in prostate cancer and benign prostate hyperplasia. However, little is known about which developmental signaling pathways guide axon investment into prostate. The first step in defining these pathways is pinpointing when axon subtypes first appear in prostate. We accomplished this by immunohistochemically mapping three axon subtypes (noradrenergic, cholinergic, and peptidergic) during fetal, neonatal, and adult stages of mouse prostate development. We devised a method for peri-prostatic axon density quantification and tested whether innervation is uniform across the proximo-distal axis of dorsal and ventral adult mouse prostate. Many axons directly interact with or innervate neuroendocrine cells in other organs, so we examined whether sensory or autonomic axons innervate neuroendocrine cells in prostate. We first detected noradrenergic, cholinergic, and peptidergic axons in prostate at embryonic day (E) 14.5. Noradrenergic and cholinergic axon densities are uniform across the proximal-distal axis of adult mouse prostate while peptidergic axons are denser in the periurethral and proximal regions. Peptidergic and cholinergic axons are closely associated with prostate neuroendocrine cells whereas noradrenergic axons are not. These results provide a foundation for understanding mouse prostatic axon development and organization and, provide strategies for quantifying axons during progression of prostate disease.
前列腺自主神经和感觉轴突控制腺体生长、液体分泌和平滑肌收缩,并在癌症和炎症期间发生重塑。在疾病进展过程中重新激活的形态发生信号通路可能驱动这种轴突重塑。这些通路与前列腺癌和良性前列腺增生中的增殖活动有关。然而,关于哪些发育信号通路引导轴突长入前列腺,我们知之甚少。定义这些通路的第一步是确定轴突亚型何时首次出现在前列腺中。我们通过免疫组织化学方法,在小鼠前列腺发育的胎儿期、新生儿期和成年期绘制了三种轴突亚型(去甲肾上腺素能、胆碱能和肽能)的图谱,从而实现了这一点。我们设计了一种前列腺周围轴突密度定量方法,并测试了成年小鼠背侧和腹侧前列腺近远轴上的神经支配是否均匀。许多轴突直接与其他器官中的神经内分泌细胞相互作用或支配这些细胞,因此我们研究了感觉或自主神经轴突是否支配前列腺中的神经内分泌细胞。我们在胚胎第14.5天首次在前列腺中检测到去甲肾上腺素能、胆碱能和肽能轴突。成年小鼠前列腺近远轴上去甲肾上腺素能和胆碱能轴突密度均匀,而肽能轴突在尿道周围和近端区域更密集。肽能和胆碱能轴突与前列腺神经内分泌细胞密切相关,而去甲肾上腺素能轴突则不然。这些结果为理解小鼠前列腺轴突的发育和组织提供了基础,并为前列腺疾病进展过程中的轴突定量提供了策略。