Induction of manganese superoxide dismutase in cultured human trophoblast during in vitro differentiation

Church, Susan L.; Farmer, Donna R.; Nelson, D. F.

doi:10.1016/0012-1606(92)90274-k

Cited by 38 publications

(16 citation statements)

References 18 publications

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“…Therefore, we used primary cultures of trophoblasts, obtained from placentas harvested after normal-term pregnancies, to examine E-cadherin expression and the role of InlA in bacterial attachment and entry. Harvested cells are known to differentiate from cytotrophoblasts to syncytiotrophoblasts over the course of a 4-day culture in DMEM supplemented with 10% FCS (15,24,25).…”

Section: Inla Mediates Bacterial Invasion Of Primary Syncytiotrophoblmentioning

confidence: 99%

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Lecuit

Nelson

Smith

et al. 2004

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

213

183

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Listeria monocytogenes produces severe fetoplacental infections in humans. How it targets and crosses the maternofetal barrier is unknown. We used immunohistochemistry to examine the location of L. monocytogenes in placental and amniotic tissue samples obtained from women with fetoplacental listeriosis. The results raised the possibility that L. monocytogenes crosses the maternofetal barrier through the villous syncytiotrophoblast, with secondary infection occurring via the amniotic epithelium. Because epidemiological studies indicate that the bacterial surface protein, internalin (InlA), may play a role in human fetoplacental listeriosis, we investigated the cellular patterns of expression of its host receptor, E-cadherin, at the maternofetal interface. E-cadherin was found on the basal and apical plasma membranes of syncytiotrophoblasts and in villous cytotrophoblasts. Established trophoblastic cell lines, primary trophoblast cultures, and placental villous explants were each exposed to isogenic InlA؉ or InlA؊ strains of L. monocytogenes, and to L. innocua expressing or not InlA. Quantitative assays of cellular invasion demonstrated that bacterial entry into syncytiotrophoblasts occurs via the apical membrane in an InlA-E-cadherin dependent manner. In human placental villous explants, bacterial invasion of the syncytiotrophoblast barrier and underlying villous tissue and subsequent replication produces histopathological lesions that mimic those seen in placentas of women with listeriosis. Thus, the InlA-E-cadherin interaction that plays a key role in the crossing of the intestinal barrier in humans is also exploited by L. monocytogenes to target and cross the placental barrier. Such a ligand-receptor interaction allowing a pathogen to specifically cross the placental villous trophoblast barrier has not been reported previously.

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Section: Inla Mediates Bacterial Invasion Of Primary Syncytiotrophoblmentioning

confidence: 99%

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Lecuit

Nelson

Smith

et al. 2004

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

213

183

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“…MnSOD is induced by mediators of oxidant stress, including tumor necrosis factor, interleukin 1, and lipopolysaccharide (23). MnSOD is also induced during normal cellular differentiation (24,25).…”

Section: Introductionmentioning

confidence: 99%

“…MnSOD Expression in Stable Transfectants and in +6 Microcell Hybrids. Detection of MnSOD sequences, SFFVneo Bluescript-specific sequences, and Cu/ZnSOD sequences were accomplished with specific 32P-labeled probes as described (24). Genomic Southern blots (29) (30).…”

mentioning

confidence: 99%

Increased manganese superoxide dismutase expression suppresses the malignant phenotype of human melanoma cells.

Church

Grant

Ridnour

et al. 1993

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

428

224

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Introduction of a normal human chromosome 6 into human melanoma cell lines results in suppression of tumorigenicity. This suggests that a gene(s) on chromosome 6 controls the malignant phenotype of human melanoma. Because antioxidants can suppress the tumor-promotion phase of carcinogenesis, and because the antioxidant enzyme manganese superoxide dismutase (MnSOD) has been localized to a region of chromosome 6 frequently lost in melanomas, we have examined the effect of transfecting sense and antisense human MnSOD cDNAs into melanoma cell lines. Cell lines expressing abundant (+)-sense MnSOD-5 cDNAs significantly altered their phenotype in culture and lost their ability to form colonies in soft agar and tumors in nude mice. In contrast, the introduction of antisense MnSOD or +psv2neo had no effect on melanoma tumorigenicity. These findings indicate that stable transfection of MnSOD cDNA into melanoma cell lines exerts a biological effect that mimics that observed after introduction of an entire human chromosome 6.

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“…Interestingly, neither the Mn SOD nor the Cu/Zn SOD isoform appeared to be present in syncytiotrophoblasts at the intensity found in the vascular endothelium and the stroma. Although this may be a relative difference in expression, this finding is surprising, given that Church et al (1992) found that in vitro differentiation of cytotrophoblasts to syncytiotrophoblasts was associated with transient expression of Mn SOD. Increased Mn SOD gene expression or enzyme activity appeared to precede or to be coordinated with morphological and biochemical trophoblast differentiation, and hence may be a marker for cell differentiation.…”

Section: Discussionmentioning

confidence: 94%

Differential Localization of Superoxide Dismutase Isoforms in Placental Villous Tissue of Normotensive, Pre-eclamptic, and Intrauterine Growth-restricted Pregnancies

Myatt

Eis

Brockman

et al. 1997

J Histochem Cytochem.

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SUMMARY Several isoforms of superoxide dismutase (SOD), including copper/zinc (cytosolic) and manganese (mitochondrial), exist. In the human placenta, SOD may prevent excessive superoxide accumulation and any potential deleterious oxidative effects. In preeclampsia, increased levels of lipid peroxide and decreased SOD activity have been described in the placenta. Oxidative stress such as occurs in pre-eclampsia can alter expression of SOD isoforms. The objective of this study was to localize the copper/zinc and manganese SOD isoforms in the placenta using immunohistochemistry and to compare localization and intensity of immunostaining in tissues from normotensive pregnancies with those from pregnancies complicated by pre-eclampsia and/or intrauterine growth restriction (IUGR). Western blotting with specific antibodies recognized a 17-kD copper/zinc and a 23-kD manganese SOD subunit in placental homogenates. Intense immunostaining for the manganese SOD isoform was seen in villous vascular endothelium, but only faint staining was found in the syncytiotrophoblast or villous stroma. In serial sections, intense immunostaining for copper/ zinc SOD was seen in certain cells of the villous stroma but only faint immunostaining in syncytiotrophoblast and vascular endothelium. No apparent differences in localization or intensity of immunostaining for either isoform were seen between tissues of normotensive or pre-eclamptic pregnancies, with or without IUGR. The different cellular localizations of the SOD isoforms suggest that they fulfill different functional roles within the placenta. I n the absence of autonomic innervation, blood flow in the human placenta must be determined by humoral mechanisms and by autocrine/paracrine factors produced in the placental vasculature itself (Myatt 1992). We have previously shown that the nitric oxide (NO) radical is a potent vasodilator of the human fetal placental vasculature in vitro (Myatt et al. 1991), where it serves to maintain basal blood flow and to attenuate the action of vasoconstrictors ). The bioactivity of NO is limited by its interaction with the superoxide anion, which causes its inactivation (Moncada et al. 1991). Conversely, the activity of NO is prolonged by the presence of the enzyme superoxide dismutase (SOD), which removes superoxide. Therefore, the bioactivity of NO may be determined by the local level of superoxide, which itself may depend on the local activity of SOD. We have shown that in the perfused human placental cotyledon, infusion of SOD into the placental fetal vasculature promotes vasodilatation (Holcberg et al. 1995b), presumably by scavenging superoxide and hence prolonging the half-life of endogenously produced NO.The action of superoxide is normally limited by its low lipid solubility, its limited membrane transport, and also by its removal by SOD, the rate constant of

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Induction of manganese superoxide dismutase in cultured human trophoblast during in vitro differentiation

Cited by 38 publications

References 18 publications

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Increased manganese superoxide dismutase expression suppresses the malignant phenotype of human melanoma cells.

Differential Localization of Superoxide Dismutase Isoforms in Placental Villous Tissue of Normotensive, Pre-eclamptic, and Intrauterine Growth-restricted Pregnancies

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