Evidence map›Paper›PMID 27388816›Full record

ArticleScientific reports2016

Caspase-3 dependent nitrergic neuronal apoptosis following cavernous nerve injury is mediated via RhoA and ROCK activation in major pelvic ganglion.

Johanna L Hannan, Hotaka Matsui, Nikolai A Sopko, Xiaopu Liu, Emmanuel Weyne, Maarten Albersen, Joseph W Watson, Ahmet Hoke, Arthur L Burnett, Trinity J Bivalacqua

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 35 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

10 authors at 4 institutions in 3 countries.

Johanna L HannanDepartment of Physiology, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC, 27834, USA.
Hotaka MatsuiDepartment of Urology, Doai Memorial Hospital and The University of Tokyo, Tokyo, Japan.
Nikolai A SopkoThe James Buchanan Brady Urological Institute, and Department of Urology, The Johns Hopkins School of Medicine, 600 North Wolfe Street, Marburg 420, Baltimore, MD, 21287, USA.
Xiaopu LiuThe James Buchanan Brady Urological Institute, and Department of Urology, The Johns Hopkins School of Medicine, 600 North Wolfe Street, Marburg 420, Baltimore, MD, 21287, USA.
Emmanuel WeyneLaboratory of Experimental Urology, Department of Urology, KU Leuven, Leuven, Belgium.
Maarten AlbersenLaboratory of Experimental Urology, Department of Urology, KU Leuven, Leuven, Belgium.
Joseph W WatsonThe James Buchanan Brady Urological Institute, and Department of Urology, The Johns Hopkins School of Medicine, 600 North Wolfe Street, Marburg 420, Baltimore, MD, 21287, USA.
Ahmet HokeDepartment of Neurology, The Johns Hopkins School of Medicine, Baltimore, MD, 21287, USA.
Arthur L BurnettThe James Buchanan Brady Urological Institute, and Department of Urology, The Johns Hopkins School of Medicine, 600 North Wolfe Street, Marburg 420, Baltimore, MD, 21287, USA.
Trinity J BivalacquaThe James Buchanan Brady Urological Institute, and Department of Urology, The Johns Hopkins School of Medicine, 600 North Wolfe Street, Marburg 420, Baltimore, MD, 21287, USA.
Johns Hopkins University · USKU Leuven · BEEast Carolina University · USThe University of Tokyo · JP

Funding

Roles of RhoA/Rho-kinase Signaling in Cavernous Neurons Following Axonal InjuryK08DK090370 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI BIVALACQUA, TRINITY JUDE · 2011 to 2015
$794k
NIDDK NIH HHS K08 DK090370
6 · The paper itself

Abstract

Axonal injury due to prostatectomy leads to Wallerian degeneration of the cavernous nerve (CN) and erectile dysfunction (ED). Return of potency is dependent on axonal regeneration and reinnervation of the penis. Following CN injury (CNI), RhoA and Rho-associated protein kinase (ROCK) increase in penile endothelial and smooth muscle cells. Previous studies indicate that nerve regeneration is hampered by activation of RhoA/ROCK pathway. We evaluated the role of RhoA/ROCK pathway in CN regulation following CNI using a validated rat model. CNI upregulated gene and protein expression of RhoA/ROCK and caspase-3 mediated apoptosis in the major pelvic ganglion (MPG). ROCK inhibitor (ROCK-I) prevented upregulation of RhoA/ROCK pathway as well as activation of caspase-3 in the MPG. Following CNI, there was decrease in the dimer to monomer ratio of neuronal nitric oxide synthase (nNOS) protein and lowered NOS activity in the MPG, which were prevented by ROCK-I. CNI lowered intracavernous pressure and impaired non-adrenergic non-cholinergic-mediated relaxation in the penis, consistent with ED. ROCK-I maintained the intracavernous pressure and non-adrenergic non-cholinergic-mediated relaxation in the penis following CNI. These results suggest that activation of RhoA/ROCK pathway mediates caspase-3 dependent apoptosis of nitrergic neurons in the MPG following CNI and that ROCK-I can prevent post-prostatectomy ED.

Indexed as

AnimalsApoptosisCaspase 3Cells, CulturedDisease Models, AnimalMaleNitrergic NeuronsPenisProstatectomyRatsRats, Sprague-Dawleyrho-Associated Kinasesrho GTP-Binding ProteinsSignal TransductionTrauma, Nervous SystemUp-RegulationCasp3 protein, ratCaspase 3RhoA protein, ratrho-Associated Kinasesrho GTP-Binding Proteins

Identifiers

PMID27388816
PMCPMC4937405
OpenAlexW2468288542

What OpenQuestion holds

Textmetadata
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.