Functional Role of Cell Surface Integrins on Human Trophoblast Cell Migration: Regulation by TGF-β, IGF-II, and IGFBP-1

Irving, J.A.; Lala, Peeyush K.

doi:10.1006/excr.1995.1105

Cited by 344 publications

(192 citation statements)

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“…Shallow trophoblast invasion is an important etiological factor in fetoplacental growth restriction. IGF-II stimulates extravillous trophoblast invasiveness primarily by promoting migration (7,25). Consistent with this finding, we have found that mature IGF-II induces HTR8͞Svneo cell migration.…”

Section: Discussionsupporting

confidence: 89%

“…Accumulated evidence suggests that IGF-II plays a key role in regulating fetoplacental growth (3)(4)(5)(6) by stimulating extravillous trophoblast migration͞invasion (7) and facilitating nutrient supply through the development of placental exchange (8). Disturbances in IGF-II expression and activity are associated with serious complications of human pregnancy, including intrauterine growth restriction (IUGR) (6,9).…”

mentioning

confidence: 99%

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Role of pro-IGF-II processing by proprotein convertase 4 in human placental development

Qiu

Basak

Mbikay

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Fetal growth restriction (intrauterine growth restriction, IUGR) is a leading cause of perinatal mortality. However, the causes of aberrant development of the placenta and, thus, of the fetus, are not currently known. Insulin-like growth factor II (IGF-II) has been shown to be an important regulator of fetoplacental growth. This growth factor must undergo posttranslational processing, and, thus, we hypothesized that aberrant processing of pro-IGF-II to IGF-II may be a cause of IUGR. Here, we have found that the proprotein convertase PC4 is expressed in the human placenta and that it cleaves pro-IGF-II to generate the intermediate processed form, IGF-II (1-102) and, subsequently, mature IGF-II (1-67), which are accounted for by the removal of terminal basic residues by carboxypeptidases. This processing confers the ability of IGF-II to activate invasive trophoblast cells through AKT phosphorylation, whereas inhibition of PC4 by a PC4-specific inhibitor blocks pro-IGF-II processing and reduces trophoblast cell migration, which can be partly restored by addition of mature IGF-II. Consistent with the hypothesis that IGF-II processing is implicated in IUGR, sera of patients carrying IUGR fetuses displayed elevated levels of pro-IGF-II. Thus, abnormal processing of IGF-II by PC4 may represent a previously uncharacterized mechanism involved in the pathophysiology of fetoplacental growth restriction, and elevated pro-IGF-II may be a useful clinical marker for risk of IUGR.insulin-like growth factor II ͉ intrauterine growth restriction

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Role of pro-IGF-II processing by proprotein convertase 4 in human placental development

Qiu

Basak

Mbikay

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Insulinlike growth factor II (IGF-II), IGF-I-binding protein I (IGFBP-I), IL-1b and EGF have all been shown to promote cytotrophoblast invasion whereas platelet-derived growth factors (PDGF-AA and PDGF-BB), vascular endothelial growth factor (VEGF), placental growth factor (PGF) and tumour necrosis factor a (TNFa) had no effect on invasion (17, 18, 28 -30). Transforming growth factor b (TGF-b) was reported to have no effect by Bass et al (17), whereas Irving & Lala (28) reported it to have a negative effect on invasion. In this study, the effects of EGF and IL-1b were consistent to other published studies on invasion.…”

Section: Discussionmentioning

confidence: 99%

The secretion and effect of inhibin A, activin A and follistatin on first-trimester trophoblasts in vitro

Bearfield¹,

Jauniaux²,

Groome

et al. 2005

eur j endocrinol

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Objective: The objectives of this study were to investigate the effect of activin A and follistatin on firsttrimester cytotrophoblast invasion in culture and to study the secretion of inhibin A, activin A and follistatin by these cells in vitro. Design and methods: Cytotrophoblasts were isolated from human placental chorionic villous tissue obtained from 6-8, 8-10 and 10 -12 weeks gestation. Cells were cultured for 3 days on cell-culture inserts coated with gelatine for invasion studies and in 24-well culture plates for secretion studies. The effects of activin A (10 ng/ml), follistatin (100 ng/ml), interleukin 1b (IL-1b; 10 ng/ml) and epidermal growth factor (EGF; 10 ng/ml) on cytotrophoblast invasion were investigated using a nonradioactive invasion assay. Secretion of inhibin A, activin A and follistatin in the presence of EGF, IL-1b, activin A and follistatin were measured using in-house ELISAs. Results and conclusion: Activin A, follistatin and EGF had a significant stimulatory effect on cytotrophoblast invasion from 6-10 weeks gestation. IL-1b had a significant stimulatory effect at 8 -10 weeks and a significant inhibitory effect on invasion at 10-12 weeks gestation. Follistatin also had a significant inhibitory effect on invasion at 10-12 weeks gestation. In the secretion study, activin A secretion at 8-10 weeks was significantly stimulated by IL-1b and EGF. At 10 -12 weeks, follistatin and EGF had a significant inhibitory effect on activin A secretion. Follistatin secretion was significantly increased in the presence of IL-1b at 6-8 weeks gestation. Inhibin A secretion was not significantly altered by EGF, IL-1b, activin A and follistatin. These results show that activin A promotes invasion of first-trimester cytotrophoblasts until 10 weeks gestation. There is a difference in the control of secretion of these proteins dependent on the gestation, suggesting that there is a tight regulation in the function of first-trimester trophoblasts depending on the gestational age.European Journal of Endocrinology 152 909-916

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“…Graham and Lala, (Graham & Lala, 1991) first demonstrated that TGF- produced primarily by the decidua inhibits trophoblast invasion. Subsequent studies revealed that TGF-3 inhibits trophoblast invasion following an interaction with endoglin, a component of the TGF-receptor complex (Caniggia et al, 1997, Irving & Lala, 1995. Recently, improved understanding of the pathogenesis of PE has raised the possibility that blood levels of antiangiogenic proteins might eventually be used to predict this devastating condition.…”

mentioning

confidence: 99%

Role of EG-VEGF in Human Placentation: Physiological and Pathological Implications

Hoffmann¹,

Brouillet²,

Benharouga³

et al. 2012

Recent Advances in Research on the Human Placenta

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Functional Role of Cell Surface Integrins on Human Trophoblast Cell Migration: Regulation by TGF-β, IGF-II, and IGFBP-1

Cited by 344 publications

References 0 publications

Role of pro-IGF-II processing by proprotein convertase 4 in human placental development

Role of pro-IGF-II processing by proprotein convertase 4 in human placental development

The secretion and effect of inhibin A, activin A and follistatin on first-trimester trophoblasts in vitro

Role of EG-VEGF in Human Placentation: Physiological and Pathological Implications

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