Evidence map›Paper›PMID 30333041›Full record

ArticleReproductive biology and endocrinology : RB&E2018

Rosiglitazone ameliorates palmitic acid-induced cytotoxicity in TM4 Sertoli cells.

Xie Ge, Peng Pan, Jun Jing, Xuechun Hu, Li Chen, Xuhua Qiu, Rujun Ma, Kadiliya Jueraitetibaike, Xuan Huang, Bing Yao

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 23 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 2 institutions in 1 country.

Xie GeCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Peng PanCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Jun JingCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Xuechun HuCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Li ChenCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Xuhua QiuCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Rujun MaCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Kadiliya JueraitetibaikeCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Xuan HuangCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China.
Bing YaoCenter of Reproductive Medicine, Nanjing Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, 210002, Jiangsu, China. yaobing@nju.edu.cn.
Nanjing University · CNNanjing General Hospital of Nanjing Military Command · CN

Funding

China Postdoctoral Science Foundation 2017M613434Family Planning Research Project of the Army 16JS012Foundation for Key Medical Talents in Jiangsu Province ZDRCA2016096Jiangsu Key Research and Development Program BE2016750National Natural Science Foundation of China 31701304National Natural Science Foundation of China 81701431National Natural Science Foundation of China 81701440Natural Science Foundation of Jiangsu Province BK20170620Six Talent Peaks Project in Jiangsu Province 2017-WSW-033
6 · The paper itself

Abstract

The Sertoli cell is the only somatic cell within the seminiferous tubules, and is vital for testis development and spermatogenesis. Rosiglitazone (RSG) is a member of the thiazolidinedione family and is a peroxisome proliferator-activated receptor-γ (PPARγ) agonist. It has been reported that RSG protects various types of cells from fatty acid-induced damage. However, whether RSG serves a protective role in Sertoli cells against palmitic acid (PA)-induced toxicity remains to be elucidated. Therefore, the aim of the present study was to investigate the effect of RSG on PA-induced cytotoxicity in Sertoli cells. MTT assay and Oil Red O staining revealed that RSG ameliorated the PA-induced decrease in TM4 cell viability, which was accompanied by an alleviation of PA-induced lipid accumulation in cells. In primary mouse Sertoli cells, RSG also showed similar protective effects against PA-induced lipotoxicity. Knockdown of PPARγ verified that RSG exerted its protective role in TM4 cells through a PPARγ-dependent pathway. To evaluate the mechanism underlying the protective role of RSG on PA-induced lipotoxicity, the present study analyzed the effects of RSG on PA uptake, and the expression of genes associated with both fatty acid oxidation and triglyceride synthesis. The results demonstrated that although RSG did not affect the endocytosis of PA, it significantly elevated the expression of carnitine palmitoyltransferase (CPT)-1A, a key enzyme involved in fatty acid oxidation, which indicated that the protective effect of RSG may have an important role in fatty acid oxidation. On the other hand, the expression of CPT1B was not affected by RSG. Moreover, the expression levels of diacylglycerol O-acyltransferase (DGAT)-1 and DGAT2, both of which encode enzymes catalyzing the synthesis of triglycerides, were not suppressed by RSG. The results indicated that RSG reduced PA-induced lipid accumulation by promoting fatty acid oxidation mediated by CPT1A. The effect of RSG in protecting cells from lipotoxicity was also found to be specific to Sertoli cells and hepatocytes, and not to other cell types that do not store excess lipid in large quantities, such as human umbilical vein endothelial cells. These findings provide insights into the cytoprotective effects of RSG on Sertoli cells and suggest that PPARγ activation may be a useful therapeutic method for the treatment of Sertoli cell dysfunction caused by dyslipidemia.

Indexed as

AnimalsCell LineCells, CulturedCell SurvivalGene ExpressionHep G2 CellsHumansHypoglycemic AgentsLipid MetabolismMaleMice, Inbred ICRPalmitic AcidPPAR gammaRNA InterferenceRosiglitazoneSertoli CellsHypoglycemic AgentsPalmitic AcidPPAR gammaRosiglitazoneCytotoxicityPalmitic acidRosiglitazoneSertoli cells

Identifiers

PMID30333041
PMCPMC6192158
OpenAlexW2896022801

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.