Galectin-1 and galectin-3 in the trophoblast of the gestational trophoblastic disease

Božić, Milica; Petronijević, Miloš; Milenković, S.; Atanacković, Jasmina; Lazić, Josipa; Vićovac, Ljiljana

doi:10.1016/j.placenta.2004.03.006

Cited by 50 publications

(42 citation statements)

References 22 publications

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“…Gal-1 was expressed by placenta [51,58], and the expression of Gal-1 was decreased in villous samples of early pregnancy loss [59], suggesting its role in sustaining normal pregnancy. Very recently, elegant work of Blois et al [52] proved that Gal-1 played a pivotal role in feto-maternal tolerance.…”

Section: Discussionmentioning

confidence: 97%

The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

Dong

Ding

Zhou

et al. 2008

Cell Physiol Biochem

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Background/Aims: Tolerance of T lymphocytes at the feto-maternal interface is necessary to sustain normal pregnancy. The present investigation aimed to observe the regulatory effects on T lymphocytes by human trophoblasts and to explore possible effector molecules. Methods: Conditioned media was made by trophoblast culture or villous explant culture for T lymphocyte proliferation and proteomic analysis. Lymphocyte proliferation was tested by thymidine incorporation. Messenger RNA for indoleamine 2,3- dioxygenase (IDO) was detected by RT-PCR and tryptophan was assayed. The protein profile of conditioned media was assessed with shotgun mass-spectrometry and the identified proteins were bioinformatically analyzed. Human chorionic gonadotropin (HCG), human chorionic somatomammotropin (HCS), interleukin (IL)-2, 4, 10 and tumor necrosis factor (TNF)- α were assayed with radioimmunoassay (RIA). Results: T Lymphocyte proliferation was inhibited by conditioned medium in a dose-dependant manner. Inhibition of IDO during previous conditioning or addition of tryptophan to the conditioned medium partly restored T lymphocyte proliferation. mRNA for IDO was expressed in trophoblasts and chorionic villi. The concentrations of tryptophan were 19.01 and 3.79 µmol/L in unconditioned and conditioned media respectively. By proteomic procedures, 548 proteins were found in placenta-conditioned medium. Among these proteins were some proteins inhibiting T lymphocytes including HCG, HCS, AFP, pregnancy-specific beta 1-glycoprotein (SP1), glycodelin, transforming growth factor β2, thrombospondin-1, pigment epithelium-derived factor (PEDF), galectin-1, and macrophage migration inhibitory factor. HCG and HCS were also detected with RIA, however, no interleukins were detected in conditioned media with RIA or proteomic analysis. Conclusions: Trophoblasts inhibit T lymphocyte through IDO-mediated tryptophan depletion and placenta-derived immunoregulatory factors. Immunological tolerance at maternal-fetal interface represents a synergistic effect of these substances and a complex mechanism involving endocrine and immune networks.

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Section: Discussionmentioning

confidence: 97%

The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

Dong

Ding

Zhou

et al. 2008

Cell Physiol Biochem

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“…34 Up-regulation of Gal-3 in both pre-eclamptic and Hemolytic anemia Elevated Liver enzymes and Low Platelet count extravillous trophoblast (EVT) may compensate for the reduced trophoblast invasion observed in both types of pathologic pregnancies. [35][36][37][38][39] Gal-4 binds to glycosphingolipids. 40,41 Furthermore, Gal-4 promotes adhesion of human colon adenocarcinoma cells.…”

Section: Role Of Galectins In Trophoblast Invasionmentioning

confidence: 99%

REVIEW ARTICLE: Governing the Invasive Trophoblast: Current Aspects on Intra‐ and Extracellular Regulation

Fitzgerald

Germeyer

Huppertz

et al. 2010

American J Rep Immunol

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Citation Fitzgerald JS, Germeyer A, Huppertz B, Jeschke U, Knöfler M, Moser G, Scholz C, Sonderegger S, Toth B, Markert UR. Governing the invasive trophoblast: current aspects on intra‐ and extracellular regulation. Am J Reprod Immunol 2010This review summarizes several aspects especially of regulating factors governing trophoblast invasion. Those include the composition of the extracellular matrix containing a variety of matrix metalloproeinases and their inhibitors, but also intracellular signals. Furthermore, a newly described trophoblast subtype, the endoglandular trophoblast, is presented. Its presence may provide a possible mechanism for opening and connecting uterine glands into the intervillous space. Amongst others, two intracellular signalling pathways are crucial for regulation of trophoblast functions and development: Wnt‐ and signal transducer and activator of transcription (STAT)3 signalling. Wnt signalling promotes implantation, placentation and trophoblast differentiation. Several Wnt‐dependent cascades and regulatory mechanisms display different functions in trophoblast cells. The STAT3 signalling system is fundamental for induction and regulation of invasiveness in physiological trophoblastic cells, but also in tumours. The role of galectins (Gal) in trophoblast regulation and placenta development comes increasingly into focus. The Gal‐ 1–4, 7–10 and 12–14 have been detected in humans. Detailed information is only available for Gal‐1, ‐2, ‐3, ‐4, ‐9 and ‐12 in endometrium and decidua. Gal‐1, ‐3 and ‐13 (‐14) have been detected and studied in trophoblast cells.

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“…It has been shown previously that expression of gal-1 is increased in choriocarcinoma (8), which may suggest an implication of this lectin in the pathology of trophoblast. However, the precise mechanisms have not been elucidated so far.…”

Section: Discussionmentioning

confidence: 69%

“…Expression or overexpression of gal-1 has been well documented in many diverse tumors, including those arising from the thy roid, endo me trium, colon, prostate, bladder, pan creas and ovary (7). It has been shown that the expression of gal-1 is increased in the transformed trophoblast of choriocarcinoma, and this finding could be related to the increased invasiveness of the transformed phenotype (8).…”

Section: Introductionmentioning

confidence: 99%

Choriocarcinoma cell line Response to Dexamethasone

Bojić‐Trbojević¹,

Kolundžić²,

Petronijević³

et al. 2010

Journal of Medical Biochemistry

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Kratak sadr`aj: Horiokarcinomske }elijske linije JAr i JEG-3 su model sistemi za ispitivanje transformisanog trofo blasta. Obe }elijske linije eksprimiraju galektin-1, ~ija je pove}ana ekspresija pokazana u horiokarcinomima u odno su na normalni trofoblast trudno}e. U ovom radu ispitivan je efekat sintetskog glukokortikoida deksametazona na JAr i JEG-3 }elijske linije, upotrebom MTT testa, ELISA testa na }elijama i testovima adhezije i migracije. Broj `ivih }elija, kao indikator proliferacije }elija, zna ~ajno je pove}an nakon tretmana 0,1 i 1 nmol/L deksameta zonom, a proliferacija JEG-3 je zna~ajno pove}ana u ~itavom opsegu upotrebljenih koncentracija deksameta zo na (0,1-100 nmol/L). Galektin-1 je u JAr moduliran deksametazonom, koji blago, ali zna~ajno smanjuje pro duk ciju galektina-1 u niskim koncentracijama (0,1 i 1 nmol/L). Kod JEG-3 }elija, produkcija galektina-1 je zna~ajno smanjena samo nakon tretmana 100 nmol/L deksameta zonom. U prisustvu laktoze kao inhibitornog {e}era za galektin-1 adhezija JEG-3 }elija je zna~ajno pove}ana, dok deksa metazon uz to smanjuje i migraciju JEG-3 }elija. Rezultati dobijeni u ovom radu po kazuju da deksametazon uti~e na proliferaciju i u manjoj meri na galektin-1 kod JAr i JEG-3 }elija, na na~in spe ci fi~an za }elijsku liniju. Dobijeni podaci ukazuju na to da bi tret man glukokortikoidima in vivo mogao imati uticaja na }elije horiokarcinoma. Summary: Choriocarcinoma cell lines JAr and JEG-3 are model systems for the study of transformed trophoblast. Both cell lines were shown to produce galectin-1, expression of which was increased in choriocarcinoma when compared to the normal trophoblast of pregnancy. In this study the effects of synthetic glucocorticoid dexamethasone were inves ti gated in both JAr and JEG-3 cell lines by the MTT test, cell based ELISA, and the cell adhesion and migration tests. Viable cell number/cell proliferation of JAr cells was signi ficantly increased after treatment with 0.1 and 1 nmol/L of dexamethasone, while proliferation of JEG-3 cells was signi ficantly increased after treatment in the whole concentration range of dexamethasone (0.1-100 nmol/L). Galectin-1 in JAr cells was modulated by dexamethasone, which mildly, but significantly decreased production at low concentrations (0.1 and 1 nmol/L). In JEG-3 cells pro duction of galectin-1 was significantly decreased only after treat ment with 100 nmol/L of dexamethasone. Cell adhe sion of JEG-3 was significantly increased in the presence of lacto se, an inhibitory sugar for gal-1, while dexamethasone indu ced decrease of JEG-3 cell migration. These findings have shown that dexamethasone may affect proliferation, gal-1 production and cell migration, in a cell line specific manner. These data suggest that glucocorticoid treatment in vivo might have the potential to affect cell functions in cho riocarcinoma.

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Galectin-1 and galectin-3 in the trophoblast of the gestational trophoblastic disease

Cited by 50 publications

References 22 publications

The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

REVIEW ARTICLE: Governing the Invasive Trophoblast: Current Aspects on Intra‐ and Extracellular Regulation

Choriocarcinoma cell line Response to Dexamethasone

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