Signal for term parturition is of trophoblast and therefore of fetal origin

Steinborn, Andrea; Güneş, Hatice; Halberstadt, E.

doi:10.1016/0090-6980(95)00138-7

Cited by 45 publications

(35 citation statements)

References 25 publications

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“…Regardless of infection status, mRNA for all three SOCS proteins were detectable in the placenta, although only SOCS1 and SOCS2 mRNAs were unequivocally detected in the membranes. Overall, SOCS protein levels were significantly higher in the preterm placenta compared with the membranes (amnion and choriodecidua), consistent with our previous findings in term tissues (Blumenstein et al 2002), and supports the notion that the placenta may have more of a role in labor-associated immune responses than previously thought (Steinborn et al 1995). These data are consistent with the work of Steinborn et al (1995) who provided evidence of placental cytokine involvement in preterm labor, both with and without intrauterine infection.…”

Section: Discussionsupporting

confidence: 83%

“…Overall, SOCS protein levels were significantly higher in the preterm placenta compared with the membranes (amnion and choriodecidua), consistent with our previous findings in term tissues (Blumenstein et al 2002), and supports the notion that the placenta may have more of a role in labor-associated immune responses than previously thought (Steinborn et al 1995). These data are consistent with the work of Steinborn et al (1995) who provided evidence of placental cytokine involvement in preterm labor, both with and without intrauterine infection. Although we have previously described the effects of labor on placental SOCS expression in term tissues, a deficiency in the present study is the lack of a non-labor control group of tissues delivered preterm.…”

Section: Discussionsupporting

confidence: 83%

“…Keelan et al (1999Keelan et al ( , 2003 found no relationship between IL-1 content and intrauterine infection in placental tissue delivered preterm. Steinborn et al (1995), in contrast, reported elevated levels of IL-1 in placental tissue cultures obtained from women without infection, but not those with confirmed chorioamnionitis, suggesting that preterm uterine activational signals are different in infected and uninfected women. The apparent discrepancy between the positive correlation between SOCS1 protein expression with IL-1 in the face of unchanged placental IL-1 levels with infection (Keelan et al , 2003 requires further elucidation.…”

Section: Discussionmentioning

confidence: 83%

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Suppressors of cytokine signaling proteins in human preterm placental tissues

Blumenstein¹,

Keelan²,

Bowen-Shauver³

et al. 2005

Journal of Molecular Endocrinology

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Decreased suppressors of cytokine signaling (SOCS) activity in human gestational tissues may play a part in the onset/progression of term labor. Since SOCS proteins negatively regulate cytokine-mediated inflammatory processes, we hypothesized that SOCS proteins are elevated in gestational tissues from spontaneous preterm deliveries with intrauterine infection. SOCS1, -2 and -3 mRNAs and proteins were detectable by RT-PCR and immunoblotting respectively, in preterm amnion, choriodecidua and placenta, irrespective of infection status. Immunoperoxidase staining localized SOCS1, -2 and -3 to all cell types of the gestational membranes, with infiltrating leukocytes reacting strongly in infected tissues. In villous placenta, SOCS was immunolocalized to the syncytiotrophoblast with marked staining of round mesenchymal cells, possibly Hofbauer cells. Nuclear SOCS staining was seen in amnion, chorion and placental syncytiotrophoblasts. SOCS proteins were, in general, significantly more abundant in placenta compared with amnion or choriodecidua. Placental SOCS1 and interleukin-1 concentrations were positively correlated (r 2 =0·47; P<0·05). However, no changes in SOCS levels in any tissues were observed with intrauterine infection. The relatively large amounts of SOCS proteins in the placenta may reflect a placenta-specific immuno-protective response to minimize the elaboration and effects of cytokines with potential to harm the placenta and fetus. Lack of labor-associated changes in SOCS levels suggests that the regulation of SOCS expression in preterm gestational tissues differs from those at term, perhaps reflecting roles in regulating placental somatotropic responses.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 83%

See 1 more Smart Citation

Suppressors of cytokine signaling proteins in human preterm placental tissues

Blumenstein¹,

Keelan²,

Bowen-Shauver³

et al. 2005

Journal of Molecular Endocrinology

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“…IL-1b and IL-8 appear to be responsible for normal cervical ripening [32]. Increased placental TNF-a, IL-1, and IL-8 have been associated with PTD that is due to other causes [32][33][34][35][36][37][38][39]. TNF-a and IL-1b may have this effect by increasing prostaglandin synthesis and efficacy [40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Malaria and Pregnancy: Placental Cytokine Expression and Its Relationship to Intrauterine Growth Retardation

et al. 1999

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Malaria infections during pregnancy can lead to the delivery of low-birth-weight infants. In this study, cytokine mRNA was measured in placentas from 23 malaria-infected and 21 uninfected primigravid women who had delivered in Mangochi, Malawi, a region with a high rate of transmission of falciparum malaria. Significantly increased expression of interleukin (IL)-1beta, IL-8, and tumor necrosis factor (TNF)-alpha and decreased expression of IL-6 and transforming growth factor-beta1 were found in malaria-infected compared with uninfected placentas. TNF-alpha and IL-8 were produced by maternally derived hemozoin-laden placental macrophages. Increased TNF-alpha expression was associated with increased placental hemozoin concentrations. Increased TNF-alpha or IL-8 expression in the placenta was associated with intrauterine growth retardation but not with preterm delivery. The results suggest that malaria infections induce a potentially harmful proinflammatory response in the placenta.

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“…There is a great body of data indicating that the content of TNF-~ in the amniotic [30] and cervicovaginal [55] fluids increases during preterm and term labors, respectively. It was also shown that activity of IL-1, IL-6, and IL-8 in the amniotic fluid increased during preterm and term labors [29,31,32].…”

mentioning

confidence: 99%