Evidence map›Paper›PMID 25891800›Full record

ArticleAndrology2015

Humanin protects against chemotherapy-induced stage-specific male germ cell apoptosis in rats.

P Surampudi, I Chang, Y Lue, T Doumit, Y Jia, V Atienza, P Y Liu, R S Swerdloff, C Wang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Andrology, 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
1.9field-weighted citation impact, top 15% 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, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Humanin analog enhances the protective effect of dexrazoxane against doxorubicin-induced cardiotoxicity.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  9. Article
  10. Article
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

9 authors at 2 institutions in 1 country.

P Surampudi *Division of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
I Chang *Division of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
Y LueDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
T DoumitDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
Y JiaDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
V AtienzaDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
P Y LiuDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
R S SwerdloffDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
C WangDivision of Endocrinology, Department of Medicine, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
The Lundquist Institute · USHarbor–UCLA Medical Center · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
ENDOCRINOLOGY, METABOLISM &NUTRITION TRAINING GRANTT32DK007571 · NIDDK · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI SWERDLOFF, RONALD SHERWIN · 1988 to 2013
$2.1M
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NCATS NIH HHS UL1 TR001881NIDDK NIH HHS T32 DK007571
6 · The paper itself

Abstract

Humanin (HN) has cytoprotective action on male germ cells after testicular stress induced by heat and hormonal deprivation. To examine whether HN has protective effects on chemotherapy-induced male germ cell apoptosis, we treated four groups of adult rats with (i) vehicle (control), (ii) HN, (iii) cyclophosphamide (CP); or (iv) HN+CP. To investigate whether the protective effects of HN on germ cells require the presence of Leydig cells, another four groups of rats were pre-treated with ethane dimethanesulfonate (EDS), a Leydig cell toxicant, to eliminate Leydig cells. After 3 days, when Leydig cells were depleted by EDS, we administered: (i) vehicle, (ii) HN, (iii) CP; or (iv) HN+CP to rats. All rats were killed 12 h after the injection of HN and/or CP. Germ cell apoptosis was detected by TUNEL assay and quantified by numerical count. Compared with control and HN (alone), CP significantly increased germ cell apoptosis; HN +CP significantly reduced CP-induced apoptosis at early (I-VI) and late stages (IX-XIV) but not at middle stages (VII-VIII) of the seminiferous epithelial cycle. Pre-treatment with EDS markedly suppressed serum and intratesticular testosterone (T) levels, and significantly increased germ cell apoptosis at the middle (VII-VIII) stages. CP did not further increase germ cell apoptosis in the EDS-pre-treated rats. HN significantly attenuated germ cell apoptosis at the middle stages in EDS pre-treated rats. To investigate whether HN has any direct effects on Leydig cell function, adult Leydig cells were isolated and treated with ketoconazole (KTZ) to block testosterone synthesis. HN was not effective in preventing the reduction of T production by KTZ in vitro. We conclude that HN decreases CP and/or EDS-induced germ cell apoptosis in a stage-specific fashion. HN acts directly on germ cells to protect against EDS-induced apoptosis in the absence of Leydig cells and intratesticular testosterone levels are very low.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCyclophosphamideIntracellular Signaling Peptides and ProteinsKetoconazoleLeydig CellsMaleMesylatesRatsRats, Sprague-DawleySpermatozoaTestosteroneApoptosis Regulatory ProteinsCyclophosphamideethylene dimethanesulfonatehumaninIntracellular Signaling Peptides and ProteinsKetoconazoleMesylatesTestosteronecyclophosphamideethane dimethanesulfonategerm cell apoptosishumaninketoconazoleLeydig cells

Identifiers

PMID25891800
PMCPMC5034733
OpenAlexW2079833189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.