Targeting Aberrantly Elevated Sialyl Lewis A as a Potential Therapy for Impaired Endometrial Selection Ability in Unexplained Recurrent Miscarriage.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2022
Historique:
received: 13 04 2022
accepted: 02 06 2022
entrez: 15 7 2022
pubmed: 16 7 2022
medline: 19 7 2022
Statut: epublish

Résumé

Carbohydrate Lewis antigens including sialyl Lewis A (sLeA), sialyl Lewis X (sLeX), Lewis X (LeX), and Lewis Y (LeY) are the commonest cell surface glycoconjugates that play pivotal roles in multiple biological processes, including cell adhesion and cell communication events during embryogenesis. SLeX, LeY, and associated glycosyltransferases ST3GAL3 and FUT4 have been reported to be involved in human embryo implantation. While the expression pattern of Lewis antigens in the decidua of unexplained recurrent miscarriage (uRM) patients remains unclear. Paraffin-embedded placental tissue slides collected from patients experiencing early miscarriages (6-12 weeks) were analyzed using immunohistochemical (IHC) and immunofluorescent (IF) staining. An IHC staining revealed that Lewis antigens are mainly expressed in the luminal and glandular epithelium, IF staining further indicated the cellular localization at the apical membrane of the epithelial cells. FUTs, ST3GALs, and NEU1 located in both stromal and epithelial cells. We have found that the expression of sLeA, LeX, FUT3/4, and ST3GAL3/4 are significantly upregulated in the RM group, while FUT1 is downregulated. SLeX, LeY, ST3GAL6, and NEU1 showed no significant differences between groups. FUT3 knockdown in RL95-2 cells significantly decreased the expression of sLeA and the spheroids adhesion to endometrial monolayer. Anti-sLeA antibody can remarkably suppress both the basal and IL-1β induced adhesion of HTR-8/SVneo spheroids to RL95-2 cells monolayer. While further flow cytometry and ICC detection indicated that the treatment of RL95-2 cells with IL-1β significantly increases the surface expression of LeX, but not sLeA. SLeA, LeX, and pertinent glycosyltransferase genes FUT1/3/4 and ST3GAL3/4 are notably dysregulated in the decidua of uRM patients. FUT3 accounts for the synthesis of sLeA in RL95-2 cells and affects the endometrial receptivity. Targeting aberrantly elevated sLeA may be a potential therapy for the inappropriate implantation in uRM.

Sections du résumé

Background
Carbohydrate Lewis antigens including sialyl Lewis A (sLeA), sialyl Lewis X (sLeX), Lewis X (LeX), and Lewis Y (LeY) are the commonest cell surface glycoconjugates that play pivotal roles in multiple biological processes, including cell adhesion and cell communication events during embryogenesis. SLeX, LeY, and associated glycosyltransferases ST3GAL3 and FUT4 have been reported to be involved in human embryo implantation. While the expression pattern of Lewis antigens in the decidua of unexplained recurrent miscarriage (uRM) patients remains unclear.
Methods
Paraffin-embedded placental tissue slides collected from patients experiencing early miscarriages (6-12 weeks) were analyzed using immunohistochemical (IHC) and immunofluorescent (IF) staining. An
Results
IHC staining revealed that Lewis antigens are mainly expressed in the luminal and glandular epithelium, IF staining further indicated the cellular localization at the apical membrane of the epithelial cells. FUTs, ST3GALs, and NEU1 located in both stromal and epithelial cells. We have found that the expression of sLeA, LeX, FUT3/4, and ST3GAL3/4 are significantly upregulated in the RM group, while FUT1 is downregulated. SLeX, LeY, ST3GAL6, and NEU1 showed no significant differences between groups. FUT3 knockdown in RL95-2 cells significantly decreased the expression of sLeA and the spheroids adhesion to endometrial monolayer. Anti-sLeA antibody can remarkably suppress both the basal and IL-1β induced adhesion of HTR-8/SVneo spheroids to RL95-2 cells monolayer. While further flow cytometry and ICC detection indicated that the treatment of RL95-2 cells with IL-1β significantly increases the surface expression of LeX, but not sLeA.
Conclusions
SLeA, LeX, and pertinent glycosyltransferase genes FUT1/3/4 and ST3GAL3/4 are notably dysregulated in the decidua of uRM patients. FUT3 accounts for the synthesis of sLeA in RL95-2 cells and affects the endometrial receptivity. Targeting aberrantly elevated sLeA may be a potential therapy for the inappropriate implantation in uRM.

Identifiants

pubmed: 35837404
doi: 10.3389/fimmu.2022.919193
pmc: PMC9273867
doi:

Substances chimiques

CA-19-9 Antigen 0
Lewis Blood Group Antigens 0
Oligosaccharides 0
FUT4 protein, human EC 2.4.1.-
Fucosyltransferases EC 2.4.1.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

919193

Informations de copyright

Copyright © 2022 Ma, Yang, Kessler, Sperandio, Mahner, Jeschke and von Schönfeldt.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Références

Am J Reprod Immunol. 1996 Mar;35(3):261-6
pubmed: 8962658
Hum Reprod Update. 2020 Apr 15;26(3):356-367
pubmed: 32103270
Am J Hum Genet. 2011 Sep 9;89(3):407-14
pubmed: 21907012
Mol Cell Biochem. 2011 Apr;350(1-2):185-92
pubmed: 21197561
J Assist Reprod Genet. 2016 May;33(5):577-580
pubmed: 26843392
Cancer Immunol Immunother. 1998 Sep;47(1):47-57
pubmed: 9755878
Reprod Biomed Online. 2003 Mar;6(2):244-56
pubmed: 12676010
Cancer Res. 1988 Jan 15;48(2):475-82
pubmed: 3335015
J Reprod Immunol. 2019 Feb;131:36-43
pubmed: 30639993
Reproduction. 2008 Jul;136(1):117-23
pubmed: 18367501
Nat Chem Biol. 2012 Jul;8(7):661-8
pubmed: 22683610
Fertil Steril. 2009 Mar;91(3):908-14
pubmed: 18402946
Int J Biochem Cell Biol. 2010 Jan;42(1):80-9
pubmed: 19781661
Lancet. 2002 Jul 13;360(9327):151-9
pubmed: 12126838
Cytokine. 2003 Aug 7;23(3):86-93
pubmed: 12906871
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai). 2002 Nov;34(6):775-9
pubmed: 12417923
FEBS Lett. 2018 Nov;592(22):3696-3707
pubmed: 30220088
Korean J Pathol. 2013 Aug;47(4):340-7
pubmed: 24009629
Biol Reprod. 2010 Feb;82(2):235-45
pubmed: 19571263
Blood. 2015 Jan 22;125(4):687-96
pubmed: 25498912
Nat Rev Dis Primers. 2020 Dec 10;6(1):98
pubmed: 33303732
Anticancer Res. 1995 Jul-Aug;15(4):1159-66
pubmed: 7653994
Placenta. 2012 Sep;33(9):696-703
pubmed: 22710193
Front Immunol. 2021 May 31;12:679424
pubmed: 34135905
Oncol Rep. 2004 Dec;12(6):1251-6
pubmed: 15547746
Mol Cancer. 2014 Sep 25;13:222
pubmed: 25255877
Hum Reprod. 2002 Aug;17(8):1959-63
pubmed: 12151421
Cell Tissue Res. 1992 Dec;270(3):425-33
pubmed: 1362525
J Immunol. 2013 Nov 1;191(9):4804-17
pubmed: 24068663
Front Oncol. 2018 Feb 23;8:39
pubmed: 29527514
Glycoconj J. 1996 Oct;13(5):769-79
pubmed: 8910004
Mol Hum Reprod. 2010 Dec;16(12):886-95
pubmed: 20847090
PLoS One. 2010 Apr 21;5(4):e10287
pubmed: 20422017
Biomed Res Int. 2013;2013:243649
pubmed: 23586024
Fertil Steril. 2011 Mar 15;95(4):1446-51.e1
pubmed: 20605574
PLoS One. 2010 Apr 21;5(4):e10258
pubmed: 20422011
Endocrinology. 2004 Aug;145(8):3850-7
pubmed: 15142989
Sci Adv. 2022 Jan 07;8(1):eabj9513
pubmed: 34995107
Science. 2019 Jun 21;364(6446):1156-1162
pubmed: 31221853
Nat Chem Biol. 2008 Dec;4(12):751-7
pubmed: 18953356
Science. 2011 Sep 23;333(6050):1761-4
pubmed: 21852454
Fertil Steril. 2016 Jan;105(1):111-8.e1-4
pubmed: 26474737
Obstet Gynecol Surv. 2013 Jun;68(6):445-66
pubmed: 23942472
Biol Reprod. 2014 Oct;91(4):98
pubmed: 25187529
Proc Natl Acad Sci U S A. 2012 May 15;109(20):7776-81
pubmed: 22547830
BMC Med. 2013 Jun 26;11:154
pubmed: 23803387
Blood. 2012 Aug 2;120(5):1015-26
pubmed: 22700726
Glycobiology. 2011 Feb;21(2):225-34
pubmed: 20876654
Blood. 2014 Sep 11;124(11):1765-76
pubmed: 25061176
Biochem Biophys Res Commun. 1993 Jul 15;194(1):375-82
pubmed: 8333853
Science. 2003 Jan 17;299(5605):405-8
pubmed: 12532021
Am J Clin Pathol. 2013 Jun;139(6):746-53
pubmed: 23690116
J Biol Chem. 2011 Jun 17;286(24):21052-61
pubmed: 21521691
Am J Pathol. 2016 Feb;186(2):297-311
pubmed: 26687991
PLoS One. 2012;7(7):e41424
pubmed: 22848492
J Reprod Immunol. 2021 Apr;144:103283
pubmed: 33545613

Auteurs

Zhi Ma (Z)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Huixia Yang (H)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Mirjana Kessler (M)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Markus Sperandio (M)

Biomedical Center (BMC), Institute for Cardiovascular Physiology and Pathophysiology, Walter Brendel Center for Experimental Medicine (WBex), Faculty of Medicine, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Sven Mahner (S)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Udo Jeschke (U)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.
Department of Obstetrics and Gynaecology, University Hospital Augsburg, Augsburg, Germany.

Viktoria von Schönfeldt (V)

Department of Obstetrics and Gynaecology, University Hospital, Ludwig-Maximilians-Universität Munich, Munich, Germany.

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