Evidence map›Paper›PMID 25237904›Full record

ArticlePloS one2014

Proteolytic activity of prostate-specific antigen (PSA) towards protein substrates and effect of peptides stimulating PSA activity.

Johanna M Mattsson, Suvi Ravela, Can Hekim, Magnus Jonsson, Johan Malm, Ale Närvänen, Ulf-Håkan Stenman, Hannu Koistinen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. KLK3 in the Regulation of Angiogenesis-Tumorigenic or Not?International journal of molecular sciences · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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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

8 authors at 4 institutions in 2 countries.

Johanna M MattssonDepartment of Clinical Chemistry, Biomedicum Helsinki, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Suvi RavelaDepartment of Clinical Chemistry, Biomedicum Helsinki, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Can HekimDepartment of Clinical Chemistry, Biomedicum Helsinki, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Magnus JonssonDepartment of Laboratory Medicine, Section for Clinical Chemistry, Lund University and Laboratory Medicine Skåne, Lund, Sweden.
Johan MalmDepartment of Laboratory Medicine, Section for Clinical Chemistry, Lund University and Laboratory Medicine Skåne, Lund, Sweden.
Ale NärvänenSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.
Ulf-Håkan StenmanDepartment of Clinical Chemistry, Biomedicum Helsinki, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Hannu KoistinenDepartment of Clinical Chemistry, Biomedicum Helsinki, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Helsinki University Hospital · FILund University · SEUniversity of Helsinki · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate-specific antigen (PSA or kallikrein-related peptidase-3, KLK3) exerts chymotrypsin-like proteolytic activity. The main biological function of PSA is the liquefaction of the clot formed after ejaculation by cleavage of semenogelins I and II in seminal fluid. PSA also cleaves several other substrates, which may explain its putative functions in prostate cancer and its antiangiogenic activity. We compared the proteolytic efficiency of PSA towards several protein and peptide substrates and studied the effect of peptides stimulating the activity of PSA with these substrates. An endothelial cell tube formation model was used to analyze the effect of PSA-degraded protein fragments on angiogenesis. We showed that PSA degrades semenogelins I and II much more efficiently than other previously identified protein substrates, e.g., fibronectin, galectin-3 and IGFBP-3. We identified nidogen-1 as a new substrate for PSA. Peptides B2 and C4 that stimulate the activity of PSA towards small peptide substrates also enhanced the proteolytic activity of PSA towards protein substrates. Nidogen-1, galectin-3 or their fragments produced by PSA did not have any effect on endothelial cell tube formation. Although PSA cleaves several other protein substrates, in addition to semenogelins, the physiological importance of this activity remains speculative. The PSA levels in prostate are very high, but several other highly active proteases, such as hK2 and trypsin, are also expressed in the prostate and may cleave protein substrates that are weakly cleaved by PSA.

Indexed as

ProteolysisFibronectinsGalectin 3HumansHuman Umbilical Vein Endothelial CellsInsulin-Like Growth Factor Binding Protein 3KineticsMaleMembrane GlycoproteinsNeovascularization, PhysiologicPeptidesProstateProstate-Specific AntigenFibronectinsGalectin 3Insulin-Like Growth Factor Binding Protein 3Membrane GlycoproteinsnidogenPeptidesProstate-Specific Antigen

Identifiers

PMID25237904
PMCPMC4169579
OpenAlexW2080113882

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.