Colombel M, Vacherot F, Diez S G, Fontaine E, Buttyan R, Chopin D
Groupe d'Etude des Tumeurs Urologiques, CHU Henri Mondor, Créteil, France.
Br J Urol. 1998 Sep;82(3):380-5. doi: 10.1046/j.1464-410x.1998.00752.x.
To determine whether benign prostatic hyperplasia (BPH) results from an imbalance between cell proliferation and apoptosis, and the extent to which the rates of these opposing processes are altered with the expression of the anti-death oncoprotein bcl-2.
Ten prostate glands from normal men (mean age 43.7 years) were sampled according to McNeal's zonal anatomy, in addition to 30 prostate adenomas obtained from prostatectomy specimens from symptomatic patients (mean age 61.4 years). Tissue samples were fixed in formalin and embedded in paraffin. Proliferation and bcl-2 expression were assessed by immunostaining using Mib-1 and anti-bcl-2 antibodies, while apoptotic bodies were specifically stained using in situ nick translation. The percentage of positive cells was determined by optical microscopy.
In normal epithelium, the rates of proliferation and apoptosis were increased in the peripheral zone (Mib-1 1.7%, apoptotic bodies 3.3%) compared with the central (0.2% vs 1.4%) and transition (0.1% vs 1.8%) zones. Proliferation was significantly greater in BPH than in normal prostate tissue (3.7%), contrasting with a stable rate of apoptosis (1.4%). In the normal prostate, bcl-2 was expressed by glandular and basal cells in the peripheral zone. In the central zone, bcl-2 was overexpressed in basal cells and in most glandular cells of the intraluminal ridges. Bcl-2 expression in the transition zone was limited to dispersed basal cells. In BPH, bcl-2 was strongly expressed by basal cells in mature glandular formations and in most cells of young small nodules.
BPH may result from both an increase of proliferation within the basal compartment and a failure of apoptosis to counterbalance basal cell proliferation. Increased expression of bcl-2 may participate in this process by blocking apoptosis.
确定良性前列腺增生（BPH）是否由细胞增殖与凋亡之间的失衡所致，以及抗死亡癌蛋白bcl-2的表达对这些相反过程速率的改变程度。
除了从有症状患者的前列腺切除标本中获取的30个前列腺腺瘤（平均年龄61.4岁）外，还根据麦克尼尔分区解剖法从正常男性（平均年龄43.7岁）的十个前列腺中取样。组织样本用福尔马林固定并石蜡包埋。使用Mib-1和抗bcl-2抗体通过免疫染色评估增殖和bcl-2表达，同时使用原位缺口平移对凋亡小体进行特异性染色。通过光学显微镜确定阳性细胞的百分比。
在正常上皮中，与中央区（0.2%对1.4%）和移行区（0.1%对1.8%）相比，外周区的增殖和凋亡速率增加（Mib-1为1.7%，凋亡小体为3.3%）。BPH中的增殖明显高于正常前列腺组织（3.7%），而凋亡速率稳定（1.4%）。在正常前列腺中，外周区的腺细胞和基底细胞表达bcl-2。在中央区，bcl-2在基底细胞和腔内嵴的大多数腺细胞中过表达。移行区的bcl-2表达仅限于分散的基底细胞。在BPH中，成熟腺结构中的基底细胞和年轻小结节的大多数细胞中bcl-2强烈表达。
BPH可能是由于基底区增殖增加以及凋亡未能平衡基底细胞增殖所致。bcl-2表达增加可能通过阻断凋亡参与这一过程。
