Excessive oxidative stress in cumulus granulosa cells induced cell senescence contributes to endometriosis-associated infertility.
Animals
Antigens, Neoplasm
/ genetics
Cell Line
Cellular Senescence
/ drug effects
Cumulus Cells
/ cytology
Disease Models, Animal
Endometriosis
/ complications
Female
Gene Expression Profiling
High-Throughput Nucleotide Sequencing
Humans
Infertility, Female
/ drug therapy
Melatonin
/ administration & dosage
Mice
Mitogen-Activated Protein Kinases
/ genetics
Ovulation Induction
Oxidative Stress
/ drug effects
Sequence Analysis, RNA
Cumulus granulosa cell
Endometriosis
Endoplasmic reticulum stress
Infertility
Oxidative stress
Senescence
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
12
12
2019
revised:
06
01
2020
accepted:
10
01
2020
pubmed:
24
1
2020
medline:
17
4
2021
entrez:
24
1
2020
Statut:
ppublish
Résumé
Endometriosis an important cause of female infertility and seriously impact physical and psychological health of patients. Endometriosis is now considered to be a public health problem that deserves in-depth investigation, especially the etiopathogenesis of endometriosis-associated infertility. We aimed to illuminate the etiopathogenesis of endometriosis-associated infertility that involve excessive oxidative stress (OS) induced pathological changes of ovary cumulus granulosa cell (GCs). Senescence-associated β-galactosidase (SA β-gal) activity in GCs from endometriosis patients, soluble isoform of advanced glycation end products receptor (sRAGE) expression in follicular fluid from endometriosis patients and differentially expressed senescence-associated secretory phenotype factors (IL-1β, MMP-9, KGF and FGF basic protein) are all useful indexes to evaluate oocyte retrieval number and mature oocyte number. RNA-sequencing and bioinformatics analysis indicated senescent phenotype of endometriosis GCs and aggravated endoplasmic reticulum (ER) stress in endometriosis GCs. Targeting ER stress significantly alleviated OS-induced GCs senescence as well as mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) reduction in GCs. Moreover, melatonin administration rescued OS-enhanced ER stress, cellular senescence, and MMP and ATP abnormities of endometriosis GCs in vitro and in vivo. In conclusion, our results indicated excessive reactive oxygen species induces senescence of endometriosis GCs via arouse ER stress, which finally contributes to endometriosis-associated infertility, and melatonin may represent a novel adjuvant therapy strategy for endometriosis-associated infertility.
Identifiants
pubmed: 31972508
pii: S2213-2317(19)31499-5
doi: 10.1016/j.redox.2020.101431
pmc: PMC6974790
pii:
doi:
Substances chimiques
Antigens, Neoplasm
0
MOK protein, human
EC 2.7.11.22
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Melatonin
JL5DK93RCL
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101431Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no conflict of interest.
Références
Fertil Steril. 2010 Jul;94(2):694-700
pubmed: 19376511
Cell. 2017 Jun 1;169(6):1000-1011
pubmed: 28575665
J Biol Chem. 2012 Jul 27;287(31):25727-40
pubmed: 22669940
Aging Cell. 2006 Oct;5(5):379-89
pubmed: 16911562
Hum Exp Toxicol. 2017 Jan;36(1):82-92
pubmed: 27022166
Hum Reprod. 1995 Jun;10(6):1563-5
pubmed: 7593539
J Pineal Res. 2017 Mar;62(2):
pubmed: 27889913
Reproduction. 2001 May;121(5):647-53
pubmed: 11427152
Aging Cell. 2015 Feb;14(1):1-7
pubmed: 25399755
J Pineal Res. 2016 Oct;61(3):253-78
pubmed: 27500468
Redox Biol. 2019 Jul;25:101047
pubmed: 30470534
Physiol Rev. 2019 Apr 1;99(2):1047-1078
pubmed: 30648461
Redox Biol. 2017 Apr;11:91-102
pubmed: 27889642
Cell Rep. 2018 Mar 27;22(13):3480-3492
pubmed: 29590617
Int J Mol Sci. 2017 Apr 08;18(4):
pubmed: 28397763
Mol Aspects Med. 2014 Aug;38:54-85
pubmed: 23796757
Neurobiol Dis. 2001 Feb;8(1):114-26
pubmed: 11162245
Hum Reprod Update. 2017 Mar 1;23(2):166-187
pubmed: 27979878
Am J Physiol Cell Physiol. 2015 Mar 15;308(6):C415-25
pubmed: 25540175
Aging Cell. 2017 Aug;16(4):615-623
pubmed: 28436203
Mol Reprod Dev. 2018 Feb;85(2):128-136
pubmed: 29247565
Cell Tissue Res. 2016 Oct;366(1):231-42
pubmed: 27250533
Fertil Steril. 2015 Feb;103(2):303-16
pubmed: 25497448
Oxid Med Cell Longev. 2017;2017:9175806
pubmed: 28808499
Mol Cancer Res. 2018 Jul;16(7):1073-1076
pubmed: 29592897
Circ Res. 2018 May 11;122(10):1460-1478
pubmed: 29748369
Nat Rev Cancer. 2014 Aug;14(8):547-58
pubmed: 25030953
Fertil Steril. 2014 Jun;101(6):1688-96
pubmed: 24661731
PLoS Biol. 2008 Dec 2;6(12):2853-68
pubmed: 19053174
Redox Biol. 2017 Apr;11:482-501
pubmed: 28086196
Nat Rev Endocrinol. 2014 May;10(5):261-75
pubmed: 24366116
Hum Reprod. 2017 Dec 1;32(12):2465-2473
pubmed: 29045673
Sci Rep. 2017 Sep 7;7(1):10824
pubmed: 28883502
J Ovarian Res. 2019 May 10;12(1):43
pubmed: 31077207
Sci Rep. 2016 Oct 12;6:35165
pubmed: 27731402
J Pineal Res. 2018 Mar;64(2):
pubmed: 29149522
Fertil Steril. 2012 Jun;97(6):1438-43
pubmed: 22440252
Trends Mol Med. 2018 Oct;24(10):871-885
pubmed: 30153969
Mol Hum Reprod. 2019 Nov 30;25(11):684-694
pubmed: 31504800
Cell Death Dis. 2019 Feb 13;10(2):144
pubmed: 30760709
J Clin Endocrinol Metab. 2014 Feb;99(2):E226-33
pubmed: 24276462
Cell Mol Life Sci. 2017 Nov;74(21):3897-3911
pubmed: 28785806
Mol Hum Reprod. 2006 Nov;12(11):655-60
pubmed: 17005595
Reprod Sci. 2014 Dec;21(12):1465-71
pubmed: 24675987