Evidence map›Paper›PMID 30538214›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Involvement of Activation of Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Regulated Kinase (ERK) Signaling Pathway in Proliferation of Urethral Plate Fibroblasts in Finasteride-Induced Rat Hypospadias.

Nini An, Jinpu Peng, Guoqing He, Xia Fan, Fei Li, Hui Chen

Open access · greenAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  5. Chitosan degradation products promote healing of burn wounds of rat skin.Frontiers in bioengineering and biotechnology · 2022
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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

6 authors at 1 institution in 1 country.

Nini AnDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Jinpu PengDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Guoqing HeDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Xia FanDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Fei LiDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Hui ChenDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China (mainland).
Guizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND We investigated the role of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signaling pathway in finasteride-induced hypospadias rats and explored the mechanisms involved. MATERIAL AND METHODS The hypospadias model was established by intragastric administration of finasteride and confirmed by hematoxylin and eosin (HE) staining. The urethral plate fibroblasts (UPF) were obtained from normal and modeled rats and identified based upon vimentin expression. Thereafter, UPF were divided into a normal control group, a model group, a model + MAPK inhibitor group, and a model + ERK inhibitor group. Cell proliferation, apoptosis, and cell cycling of UPF were assessed. Quantitative real-time PCR and Western blot analysis were used to evaluate expression of the MAPK signaling pathway and apoptosis-related genes. RESULTS HE staining confirmed that 10 mg/kg finasteride caused severe hypospadias in rats. UPFs obtained from the 10 mg/kg finasteride group showed higher proliferation and cell cycling and lower apoptosis compared with those obtained from the normal control group (P<0.05). Interestingly, a MAPK inhibitor or an ERK inhibitor could attenuate the abnormalities of cell proliferation, cycling, and apoptosis of UPF induced by finasteride. Compared with controls, the relative expression of p-MEK1/MEK1, caspase 3, and P53 in the UPF of the model group were reduced, while the relative expression of p-MAPK14/MAPK14 was increased in the cells of the model group. By contrast, a MAPK inhibitor or an ERK inhibitor could alleviate the abnormalities of MAPK/ERK signaling pathway and apoptosis-related gene expression induced by finasteride. CONCLUSIONS Our study reveals that the MAPK/ERK signaling pathway is involved in the regulation of proliferation, apoptosis, and cell cycling of UPFs in finasteride-induced hypospadias.

Indexed as

AnimalsApoptosisCell ProliferationDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFibroblastsFinasterideHypospadiasMaleMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1RatsSignal TransductionUrethraExtracellular Signal-Regulated MAP KinasesFinasterideMitogen-Activated Protein Kinase 1

Identifiers

PMID30538214
PMCPMC6299793
OpenAlexW2905200345

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.