Cytokine Expression by Models of Human Trophoblast as Assessed by a Semiquantitative Reverse Transcription‐Polymerase Chain Reaction Technique

Bennett, William A.; Lagoo‐Deenadayalan, Sandhya; Brackin, Martha N.; Hale, Enatra; Cowan, Bryan D.

doi:10.1111/j.1600-0897.1996.tb00178.x

Cited by 57 publications

(33 citation statements)

References 20 publications

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“…Determination of TNFa mRNA levels by RT-PCR has previously been used for estimating the TNFa expression by human trophoblasts (King et al 1995, Bennett et al 1996. Comparing expression of TNFa mRNA on cultured CT at a pO 2 of 38 mmHg with that at 140 mmHg, we found that cells from an uncomplicated placenta expressed significantly less (P!0.05, a 35% decrease) at 38 mmHg and that IUGR cells expressed more (P!0.05, a 55% increase) at 38 mmHg.…”

Section: Discussionmentioning

confidence: 99%

Endogenous tumor necrosis factor α mediates enhanced apoptosis of cultured villous trophoblasts from intrauterine growth-restricted placentae

Kilani

Macková²,

Davidge³

et al. 2007

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Tumor necrosis factor α (TNFα) has been implicated in the abnormally high levels of trophoblast apoptosis seen in placentae from pregnancies complicated by small births. We examined the hypothesis that at physiological (35–50 mmHg) oxygen tensions, the production of TNFα stimulates the apoptosis of placental trophoblasts associated with infants that are intrauterine growth-restricted (IUGR). Highly purified cytotrophoblasts (CT) from IUGR-complicated pregnancies spontaneously underwent a higher rate of apoptosis after 24 h of culture at a normoxic (for villous CT) tension of 38 mmHg than did CT from normal placentae. Real-time PCR analysis of TNFαmRNA revealed ~threefold higher levels in IUGR trophoblasts afterculturing at a pO2of 38 mmHg. A higher level of TNFα receptor p55 (which mediates apoptosis) was found in IUGR CT by western blot analysis at pO2of <10, 38, and 140 mmHg. Neutralizing antibody to TNFα significantly inhibited the apoptosis of IUGR trophoblasts cultured at 38 mmHg and addition of TNFα significantly elevated apoptosis of normal and IUGR trophoblasts but less in IUGR cells cultured at <10 mmHg. We conclude that at physiological oxygen tensions (38 mmHg), villous CT from IUGR pregnancies, when compared with uncomplicated pregnancies, undergo more TNFα-induced apoptosis both because of elevated expression of TNFα and TNF receptor p55.

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Section: Discussionmentioning

confidence: 99%

Endogenous tumor necrosis factor α mediates enhanced apoptosis of cultured villous trophoblasts from intrauterine growth-restricted placentae

Kilani

Macková²,

Davidge³

et al. 2007

Reproduction

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“…44 As we described previously, FK-stimulated BeWo cells also express markers of typical syncytiotrophoblast cells, such as human chorionic gonadotrophin and markedly reduced E-cadherin expression. 38 Moreover, BeWo cells express IL-10 at the mRNA and the protein levels 45,46 and a recent study demonstrated that this cell line responds very well to exogenous IL-10. 47 Thus, these similarities to trophoblast cells support the use of BeWo cells as a valid and suitable model for studying different aspects of villous cytotrophoblast differentiation and function.…”

Section: Isolation and Purification Of Term Villous Cytotrophoblastsmentioning

confidence: 99%

The activating effect of IFN-γ on monocytes/macrophages is regulated by the LIF–trophoblast–IL-10 axis via Stat1 inhibition and Stat3 activation

et al. 2014

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Interferon gamma (IFN-c) and leukemia inhibitory factor (LIF) are key gestational factors that may differentially affect leukocyte function during gestation. Because IFN-c induces a pro-inflammatory phenotype in macrophages and because trophoblast cells are principal targets of LIF in the placenta, we investigated whether and how soluble factors from trophoblast cells regulate the effects of IFN-c on macrophage activation. IFN-c reduces macrophage motility, but enhances Stat1 activation, pro-inflammatory gene expression and cytotoxic functions. Soluble factors from villous cytotrophoblasts (vCT1LIF cells) and BeWo cells (BW/ST1LIF cells) that were differentiated in the presence of LIF inhibit macrophage Stat1 activation but inversely sustain Stat3 activation in response to IFN-c. vCT1LIF cells produce soluble factors that induce Stat3 activation; this effect is partially abrogated in the presence of neutralizing anti-interleukin 10 (IL-10) antibodies. Moreover, soluble factors from BW/ST1LIF cells reduce cell proliferation but enhance the migratory responses of monocytes. In addition, these factors reverse the inhibitory effect of IFN-c on monocyte/macrophage motility. BW/ST1LIF cells also generate IFN-c-activated macrophages with enhanced IL-10 expression, but reduced tumor-necrosis factor alpha (TNF-a), CD14 and CD40 expression as well as impaired cytotoxic function. Additional assays performed in the presence of neutralizing anti-IL-10 antibodies and exogenous IL-10 demonstrate that reduced macrophage cytotoxicity and proliferation, but increased cell motility result from the ability of trophoblast IL-10 to sustain Stat3 activation and suppress IFN-c-induced Stat1 activation. These in vitro studies are the first to describe the regulatory role of the LIF-trophoblast-IL-10 axis in the process of macrophage activation in response to pro-inflammatory cytokines.

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“…As it is known that upregulation of Th1 activity responses was also shown in vitro by increased IFN-␥ [20]. Increased concentrations of this cytokine are harmful for pregnancy, causing fetal resorption in a murine model of recurrent spontaneous abortion [25], and could also be responsible for induction of trophoblast apoptosis [26]. Indeed, NO inhibits the secretion of IFN-␥ by Th1 cells [27].…”

Section: Discussionmentioning

confidence: 98%

Intergenotypic variation of nitric oxide and inflammatory markers in preeclampsia: A pilot study in a North Indian population

et al. 2011

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Cytokine Expression by Models of Human Trophoblast as Assessed by a Semiquantitative Reverse Transcription‐Polymerase Chain Reaction Technique

Abstract: Human choriocarcinoma cells and term trophoblast express cytokines that may regulate critical reproductive events. Expression of inflammatory cytokines such as IL-1, TNF-alpha, and IFN-gamma by term trophoblast could trigger labor or be a consequence of labor-associated events.

Cited by 57 publications

References 20 publications

Endogenous tumor necrosis factor α mediates enhanced apoptosis of cultured villous trophoblasts from intrauterine growth-restricted placentae

Endogenous tumor necrosis factor α mediates enhanced apoptosis of cultured villous trophoblasts from intrauterine growth-restricted placentae

The activating effect of IFN-γ on monocytes/macrophages is regulated by the LIF–trophoblast–IL-10 axis via Stat1 inhibition and Stat3 activation

Intergenotypic variation of nitric oxide and inflammatory markers in preeclampsia: A pilot study in a North Indian population

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