Evidence map›Paper›PMID 25763122›Full record

ArticleKorean journal of urology2015

Structural modifications of the prostate in hypoxia, oxidative stress, and chronic ischemia.

Portia Thurmond, Jing-Hua Yang, Yedan Li, Lori B Lerner, Kazem M Azadzoi

Open access · diamondAbstract read
In one paragraph

Article in Korean journal of urology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Portia ThurmondDepartment of Urology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
Jing-Hua YangDepartment of Urology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
Yedan LiDepartment of Urology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
Lori B LernerDepartment of Urology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
Kazem M AzadzoiDepartment of Urology and Department of Pathology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
Boston University · USVA Boston Healthcare System · US

Funding

Mechanism of Bladder Overactivity in Pelvic IschemiaI01BX001428 · VA · VA BOSTON HEALTH CARE SYSTEM · PI AZADZOI, KAZEM M · 2013 to 2016
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BLRD VA I01 BX001428
6 · The paper itself

Abstract

purposeClinical studies have reported a correlation between pelvic ischemia and voiding dysfunction in elderly men. The aim of this study was to identify and compare prostate structural modifications in cultured cells and in a rabbit model after exposure to hypoxia, oxidative stress, and chronic ischemia. MATERIALS AND

methodsCultured human prostate smooth muscle cells (SMCs), epithelial cells (ECs), and stromal cells (SCs) were incubated under normoxia, hypoxia, and oxidative stress conditions by use of a computerized oxycycler system. We developed a rabbit model of chronic prostate ischemia by creating aorto-iliac arterial atherosclerosis. Markers of oxidative stress were examined by using fluorometric analysis and enzyme immunoassay. Prostate structure was examined by using Masson's trichrome staining and transmission electron microscopy (TEM).

resultsLipid peroxidation was found in SMCs exposed to hypoxia and in all cell types exposed to oxidative stress. We identified protein oxidation in ECs exposed to hypoxia and in all cell types exposed to oxidative stress. Markers indicating oxidative damage were present in chronically ischemic rabbit prostate tissue. These reactions were associated with DNA damage. Prostate ischemia resulted in epithelial atrophy, loss of smooth muscle, and diffuse fibrosis. TEM showed swollen mitochondria with degraded cristae, loss of membrane, loss of Golgi bodies, degenerated nerves, and disrupted cell-to-cell junctions.

conclusionsHuman prostate cells exhibited differential reactions to hypoxia and oxidative stress with widespread DNA damage. Structural modifications in ischemic prostate tissue were similar to those in cells exposed to oxidative stress. Structural changes due to ischemia and oxidative stress may contribute to prostatic noncompliance in aging men.

Indexed as

Oxidative StressAnimalsAtherosclerosisBiomarkersCells, CulturedDisease Models, AnimalDNA DamageEpithelial CellsFibrosisHumansHypoxiaIschemiaLipid PeroxidationMaleMyocytes, Smooth MuscleNerve DegenerationBiomarkersFibrosisIschemiaOxidative stressProstate

Identifiers

PMID25763122
PMCPMC4355429
OpenAlexW2075930427

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.