Basic scienceApoptosis profiles in benign prostatic hyperplasia: Close associations of cell kinetics with percent area density of histologic composition
Section snippets
Material and methods
This study included 60 patients with BPH who underwent transurethral resection of the prostate or suprapubic prostatectomy. Their age range was 59 to 76 years (median age 66). None of these patients had undergone previous hormonal manipulation. The formalin-fixed and paraffin-embedded specimens were cut into 5-μm-thick sections and placed on Poly-l-lysine-treated glass slides. For histopathologic examination, each paraffin block was step sectioned and routinely stained with hematoxylin-eosin
Percent Area Density
The average percent area density of epithelium, stroma, and lumen was 14.4% ± 4.1%, 75.5% ± 10.7%, and 10.1% ± 5.9 %, respectively. The ratio of stroma to epithelium ranged from 4.6:1 to 6.3:1 (average 5.2:1) in BPH specimens. The percent area density of epithelium and stroma was not related to patient age or prostate volume.
Apoptotic and Proliferation Indexes
Both TUNEL-positive cells and Ki-67-positive cells were detected in the glandular cells and stromal cells of BPH (Fig. 1A,B). The average PI and AI were 1.8 and 0.7 in the
Comment
It is known that human BPH is the result of proliferation of the stromal and epithelial compartments. This proliferation begins in the stroma, with proliferation of the glandular epithelium secondarily induced.1 A number of studies have shown close associations between the development and severity of clinical BPH and the cellular composition of the prostate.17, 18 It is clear that the proportion of stromal components is absolutely greater than that of epithelial compartments in human BPH.
Conclusions
This is the first study to examine correlations of apoptosis and apoptosis-associated factors with the percent area density of epithelial and stromal components in BPH. Our data showed a close relation of a greater PI to the percent area density of stroma and an inverse relation of a greater AI to the percent area density of epithelium in BPH tissue. The development of BPH may be associated with both stromal growth, due to active mesenchymal-stromal cell proliferation, and epithelial growth,
References (23)
- et al.
Cell kinetics in epithelium and stroma of benign prostatic hyperplasia
J Urol
(1997) - et al.
Apoptotic versus proliferative activities in human benign prostatic hyperplasia
Hum Pathol
(1996) - et al.
C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2
Cell
(1994) - et al.
The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme
Cell
(1993) - et al.
DFF, a heterodimeric protein that functions downstream of caspase-3 to trigger DNA fragmentation during apoptosis
Cell
(1997) - et al.
Expression of survivin and apoptotic biomarkers in benign prostatic hyperplasia
J Urol
(2005) - et al.
p53 accumulation associated with bcl-2, the proliferation marker MIB-1 and survival in patients with prostate cancer subjected to watchful waiting
J Urol
(2000) - et al.
Biological feature of prostatic hyperplasia developed in spontaneously hypertensive rats
Urology
(2004) - et al.
The relative proportion of stromal and epithelial hyperplasia is related to the development of symptomatic benign prostate hyperplasia
J Urol
(1992) - et al.
Characterization and localization of nitric oxide synthase in the human prostate
Urology
(1995)
Pathology of benign prostatic hyperplasia
Prostate Suppl
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2022, Life SciencesCitation Excerpt :Furthermore, a chronic inflammatory condition may play an important part in BPH progression and prostate cancer by causing tissue injury that stimulates prostatic cell proliferation [14]. These incidences reflect a difference between cell death and proliferation, resulting in a rise in BPH [15]. In the pathophysiology of BPH, growth factors linked with cellular proliferation, differentiation, apoptosis, and epithelial/stromal interaction have been reported [16].
Chinese Skullcap (Scutellaria baicalensis Georgi) inhibits inflammation and proliferation on benign prostatic hyperplasia in rats
2019, Journal of EthnopharmacologyCitation Excerpt :Recurrent tissue damage owing to chronic inflammation leads to compensated cellular proliferation, which results in hyperplasia (Chughtai et al., 2011; Sciarra et al., 2007). This event also induces disproportion between cell proliferation and apoptosis and leads to the occurrence of BPH (Zhang et al., 2006). Previous study identified that the apoptotic extent of prostate epithelium cells was higher in the normal tissue than in the hyperplastic prostate, whereas there was a significant augment in the proliferative cell proportions in the BPH tissue (Kyprianou et al., 1996).
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2009, Journal of UrologyCitation Excerpt :Recently it was indicated that an imbalance between apoptosis and cell proliferation may underlie BPH development.11 The development of human BPH may be associated with stromal growth due to active mesenchymal-stromal cell proliferation and with an epithelial increment due to decreased glandular apoptosis.12 It is possible that endogenous hormone has some role in these responses because the prostate gland is androgen dependent, in that it requires testosterone for growth, development, differentiation and function, while androgen deprivation decreases the size of the prostate.