Murray Elaine, Malley Susan E, Qiao Li-Ya, Hu Vivian Y, Vizzard Margaret A
Department of Neurology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA.
J Urol. 2004 Dec;172(6 Pt 1):2434-9. doi: 10.1097/01.ju.0000143549.29867.4e.
We examined neurotrophin and receptor tyrosine kinase (Trk) expression in the bladder and major pelvic ganglia (MPG) after cyclophosphamide induced cystitis in rats.
The bladder and MPG were used in immunohistochemical studies, enzyme-linked immunoassays and Western blots for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), TrkA and TrkB. Bladder postganglionic MPG cells were labeled by tracing techniques.
NGF and BDNF expression was decreased in the bladder of all rats after cystitis (p < or =0.001). NGF and BDNF expression was increased in the MPG in male rats with cystitis (p < or =0.01). Cells expressing TrkA and TrkB immunoreactivity (IR) increased 78% to 81% in the MPG in male rats with cystitis. TrkA-IR or TrkB-IR bladder postganglionic cells increased 50% to 74% with cystitis. Cystitis increased TrkA-IR 5 to 10-fold and TrkB-IR 10 to 12-fold in detrusor muscle. TrkA-IR and TrkB-IR were prominent in control urothelium but decreased with cystitis. After cystitis TrkB-IR nerve fibers and TrkA-IR cellular infiltrates were more apparent compared to controls.
Cystitis decreases bladder NGF and BDNF expression, whereas MPG expression is increased. This change may reflect neurotrophin release at the bladder and retrograde transport to the MPG. TrkA-IR and TrkB-IR are increased in bladder postganglionic cells and bladders with cystitis. This increase may reflect a shift in Trk staining from urothelium to detrusor muscle and nerve fibers with cystitis. Neurotrophin/Trk interactions in the bladder and MPG may contribute to bladder overactivity with cystitis.
我们研究了环磷酰胺诱导大鼠膀胱炎后膀胱和主要盆神经节（MPG）中神经营养因子和受体酪氨酸激酶（Trk）的表达。
将膀胱和MPG用于免疫组织化学研究、酶联免疫吸附测定以及针对神经生长因子（NGF）、脑源性神经营养因子（BDNF）、TrkA和TrkB的蛋白质印迹分析。通过追踪技术标记膀胱节后MPG细胞。
膀胱炎后所有大鼠膀胱中NGF和BDNF表达均降低（p≤0.001）。膀胱炎雄性大鼠的MPG中NGF和BDNF表达增加（p≤0.01）。膀胱炎雄性大鼠的MPG中表达TrkA和TrkB免疫反应性（IR）的细胞增加了78%至81%。膀胱炎时，TrkA-IR或TrkB-IR膀胱节后细胞增加了50%至74%。膀胱炎使逼尿肌中TrkA-IR增加5至10倍，TrkB-IR增加10至12倍。TrkA-IR和TrkB-IR在对照尿路上皮中显著，但膀胱炎后降低。与对照相比，膀胱炎后TrkB-IR神经纤维和TrkA-IR细胞浸润更明显。
膀胱炎降低膀胱NGF和BDNF表达，而MPG表达增加。这种变化可能反映神经营养因子在膀胱释放并逆行转运至MPG。膀胱炎时膀胱节后细胞和膀胱中TrkA-IR和TrkB-IR增加。这种增加可能反映膀胱炎时Trk染色从尿路上皮向逼尿肌和神经纤维的转变。膀胱和MPG中的神经营养因子/Trk相互作用可能导致膀胱炎时膀胱过度活动。
