Evidence map›Paper›PMID 27114192›Full record

ArticleThe journal of sexual medicine2016

Implanted Muscle-Derived Stem Cells Ameliorate Erectile Dysfunction in a Rat Model of Type 2 Diabetes, but Their Repair Capacity Is Impaired by Their Prior Exposure to the Diabetic Milieu.

Istvan Kovanecz, Dolores Vernet, Maryam Masouminia, Robert Gelfand, Leila Loni, James Aboagye, James Tsao, Jacob Rajfer, Nestor F Gonzalez-Cadavid

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The journal of sexual medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Istvan KovaneczDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA; Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Dolores VernetDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
Maryam MasouminiaDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
Robert GelfandDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA; Department of Medicine, Charles Drew University of Medicine and Science, Los Angeles, CA, USA.
Leila LoniDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA.
James AboagyeDepartment of Medicine, Charles Drew University of Medicine and Science, Los Angeles, CA, USA.
James TsaoDepartment of Medicine, Charles Drew University of Medicine and Science, Los Angeles, CA, USA.
Jacob RajferDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA; Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Nestor F Gonzalez-CadavidDivision of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA; Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; Department of Medicine, Charles Drew University of Medicine and Science, Los Angeles, CA, USA. Electronic address: ncadavid@ucla.edu.
Charles R. Drew University of Medicine and Science · USTorrance Memorial Medical Center · USHarbor–UCLA Medical Center · USThe Lundquist Institute · USUniversity of California, Los Angeles · US

Funding

Coordinating and Bioinformatics Unit for the MMPC/DiaCompU24DK076169 · NIDDK · AUGUSTA UNIVERSITY · PI MCINDOE, RICHARD A. · 2006 to 2018
$42.4M
The CDU-Clinical Research Education and Career Development ProgramR25MD007610 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Roberto Balbino Vargas · 2012 to 2026
$7.8M
NIDDK NIH HHS U24 DK076169NIMHD NIH HHS R25 MD007610
6 · The paper itself

Abstract

introductionMuscle-derived stem cells (MDSCs) and other SCs implanted into the penile corpora cavernosa ameliorate erectile dysfunction in type 1 diabetic rat models by replenishing lost corporal smooth muscle cells (SMCs) and decreasing fibrosis. However, there are no conclusive data from models of type 2 diabetes (T2D) and obesity.

aimTo determine whether MDSCs from obese Zucker (OZ) rats with T2D at an early stage of diabetes (early diabetic SCs isolated and cultured in low-glucose medium [ED-SCs]) counteract corporal veno-occlusive dysfunction and corporal SMC loss or lipo-fibrosis when implanted in OZ rats at a late stage of diabetes and whether MDSCs from these OZ rats with late diabetes (late diabetic SCs isolated and cultured in high-glucose medium [LD-SC]) differ from ED-SCs in gene transcriptional phenotype and repair capacity.

methodsED-SCs and LD-SCs were compared by DNA microarray assays, and ED-SCs were incubated in vitro under high-glucose conditions (ED-HG-SC). These three MDSC types were injected into the corpora cavernosa of OZ rats with late diabetes (OZ/ED, OZ/LD, and OZ/ED-HG rats, respectively). Untreated OZ and non-diabetic lean Zucker rats functioned as controls. Two months later, rats were subjected to cavernosometry and the penile shaft and corporal tissues were subjected to histopathology and DNA microarray assays.

main outcome measuresIn vivo erectile dysfunction assessment by Dynamic Infusion Cavernosometry followed by histopathology marker analysis of the penile tissues.

resultsImplanted ED-SCs and ED-HG-SCs improved corporal veno-occlusive dysfunction, counteracted corporal decreases in the ratio of SMCs to collagen and fat infiltration in rats with long-term T2D, and upregulated neuronal and endothelial nitric oxide. LD-SCs acquired an inflammatory, pro-fibrotic, oxidative, and dyslipidemic transcriptional phenotype and failed to repair the corporal tissue.

conclusionMDSCs from pre-diabetic rats injected into the corpora cavernosa of rats with long-term T2D improve corporal veno-occlusive dysfunction and the underlying histopathology. In contrast, MDSCs from rats with long-term uncontrolled T2D are imprinted by the hyperglycemic and dyslipidemic milieu with a noxious phenotype associated with an impaired tissue repair capacity. SCs affected by diabetes could lack tissue repair efficacy as autografts and should be reprogrammed in vitro or substituted by SCs from allogenic non-diabetic sources.

Indexed as

Stem Cell TransplantationAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2EndotheliumErectile DysfunctionMaleMyocytes, Smooth MusclePenisRatsRats, ZuckerStem CellsCorpora CavernosaCorporal Veno-Occlusive DysfunctionDiabetesDyslipidemiaFibrosisHyperglycemiaMyostatinObesitySmooth MuscleStem Cell Damage

Identifiers

PMID27114192
PMCPMC4886867
OpenAlexW2338492788

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.