Evidence map›Paper›PMID 36849880›Full record

ArticleCellular & molecular biology letters2023

The RXFP2-PLC/PKC signaling pathway mediates INSL3-induced regulation of the proliferation, migration and apoptosis of mouse gubernacular cells.

Shouxing Duan, Xuewu Jiang, Jianhong Li, Maxian Fu, Zhuo Li, Yiyi Cheng, Yangmu Zhuang, Ming Yang, Wenfeng Xiao, Hongyan Ping and 3 more

Open access · goldAbstract readLetter
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

3 citing papers in PubMed, 8 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

13 authors at 4 institutions in 1 country.

Shouxing DuanDepartment of Pediatric Surgery, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), No. 89 Taoyuan Road, Shenzhen, 518052, Guangdong, China.
Xuewu JiangDepartment of Pediatric Surgery, Pingshan District Maternal and Child Healthcare Hospital of Shenzhen, Pingshan General Hospital of Southern Medical University, No. 6 Longxingnan Road, Shenzhen, 518118, Guangdong, China.
Jianhong LiDepartment of Pediatric Surgery, The Second Affiliated Hospital of Shantou University Medical College, No. 69 Dongxiabei Road, Shantou, 515041, Guangdong, China.
Maxian FuDepartment of Pediatric Surgery, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), No. 89 Taoyuan Road, Shenzhen, 518052, Guangdong, China.
Zhuo LiDepartment of Pediatric Surgery, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), No. 89 Taoyuan Road, Shenzhen, 518052, Guangdong, China.
Yiyi ChengDepartment of Pediatric Surgery, The First Affiliated Hospital of Shantou University Medical College, No. 57 Changping Road, Shantou, 515041, Guangdong, China.
Yangmu ZhuangDepartment of Pediatric Surgery, The First Affiliated Hospital of Shantou University Medical College, No. 57 Changping Road, Shantou, 515041, Guangdong, China.
Ming YangDepartment of Pediatric Surgery, The First Affiliated Hospital of Shantou University Medical College, No. 57 Changping Road, Shantou, 515041, Guangdong, China.
Wenfeng XiaoDepartment of Pediatric Surgery, The Second Affiliated Hospital of Shantou University Medical College, No. 69 Dongxiabei Road, Shantou, 515041, Guangdong, China.
Hongyan PingDepartment of Pediatric Surgery, Pingshan District Maternal and Child Healthcare Hospital of Shenzhen, Pingshan General Hospital of Southern Medical University, No. 6 Longxingnan Road, Shenzhen, 518118, Guangdong, China.
Yao XieDepartment of Radiology, Cancer Hospital of Shantou University Medical College, No. 7 Raoping Road, Shantou, 515041, Guangdong, China. stxieyao@163.com.ORCID http://orcid.org/0000-0002-3539-6741
Xiaojun XieDepartment of General Surgery, The First Affiliated Hospital of Shantou University Medical College, No. 57 Changping Road, Shantou, 515041, Guangdong, China. xjxie79@163.com.
Xuan ZhangDepartment of Pediatric Surgery, Pingshan District Maternal and Child Healthcare Hospital of Shenzhen, Pingshan General Hospital of Southern Medical University, No. 6 Longxingnan Road, Shenzhen, 518118, Guangdong, China. zhxuan2006@126.com.
Shantou University · CNHuazhong University of Science and Technology · CNSouthern Medical University · CNShenzhen Maternity and Child Healthcare Hospital · CN

Funding

National Natural Science Foundation of China 81801432Natural Science Foundation of Guangdong Province of China 2018A030307045Natural Science Foundation of Guangdong Province of China 2022A1515010407
6 · The paper itself

Abstract

backgroundTesticular hypoplasia can affect the sexual and reproductive ability in adulthood, and even increase the risk of cancer. Abnormal development of the gubernaculum is one of the important factors of testicular hypoplasia. Therefore, a study of the structure and function of the gubernaculum is an important but neglected new breakthrough point for investigating the normal/abnormal development of the testis. Previous findings showed that Insulin like factor 3 (INSL3) is a key factor regulating the growth of gubernaculum, however, the mechanism by which INSL3 acts on the gubernaculum remains unknown. Therefore, we probed the mechanism associated with INSL3-induced the proliferation, migration, and apoptosis of gubernacular cells in mice.

methodsA culture cell model of neonatal mice gubernaculum is established by INSL3 intervention. We blocked PLC/PKC signaling pathway with U73122 pretreat to investigate the role of the PLC/PKC signaling pathway. The changes of cell proliferation, migration, and apoptosis were detected by molecular biological methods. In addition, the levels of PCNA and F-action were detected by immunofluorescence and western blotting.

resultsWe found that INSL3 can promote the proliferation and migration of gubernacular cells and inhibit their apoptosis, meanwhile, INSL3 significantly up-regulated PLC/PKC protein phosphorylation. However, treatment with the PLC/PKC signaling pathway inhibitor U73122 significantly inhibited these effects of INSL3. Besides, we found that INSL3 could up-regulate the protein expression level of PCNA and F-actin, while the PCNA and F-actin expression was significantly weakened after U73122 pretreatment.

conclusionsThis research revealed that INSL3 binding to RXFP2 may up-regulate the expression levels of PCNA and F-actin by activating the PLC/PKC signaling pathway to promote the proliferation and migration of gubernacular cells. It suggests that the RXFP2-PLC/PKC axis may serve as a novel molecular mechanism by which INSL3 regulates growth of the gubernaculum.

Indexed as

ActinsGubernaculumAnimalsApoptosisCell ProliferationInsulinMaleMiceProliferating Cell Nuclear AntigenProteinsReceptors, G-Protein-CoupledSignal TransductionType C PhospholipasesActinsInsulinLeydig insulin-like proteinProliferating Cell Nuclear AntigenProteinsReceptors, G-Protein-CoupledRXFP2 protein, mouseType C PhospholipasesGubernaculumINSL3PLC/PKCRXFP2Signaling pathway

Identifiers

PMID36849880
PMCPMC9972740
OpenAlexW4322491754

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.