Decidual Activin: Its Role In the Apoptotic Process and Its Regulation by Prolactin1

Tessier, C.; Prigent‐Tessier, Anne; Bao, Lei; Telleria, Carlos; Ferguson-Gottschall, Susan; Gibori, Gil B.; Gu, Yun; Bowen-Shauver, Jennifer M.; Horseman, Nelson D.; Gibori, Geula

doi:10.1095/biolreprod.102.011684

Cited by 23 publications

(17 citation statements)

References 41 publications

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“…The neurotrophic function of activin A after hypoxic-ischemic brain injury (11,(22)(23)(24)(25) enhances the survival of midbrain and hippocampal neurons (24,25 ), decreases ischemic brain injury in infant rats (11 ), and shields striatal and midbrain neurons against neurotoxic damage (22,23,25 ). These findings and the evidence that activin A prevents apoptosis (26 ) and inhibits caspase (27 ), 2 important pathways involved in neuronal death (28 ), support the hypothesis that oversecretion of activin A in the presence of hypoxia/asphyxia may serve a neuroprotective function, reducing neuronal Clinical Chemistry 52, No. 8,2006 loss from brain injury.…”

Section: Discussionmentioning

confidence: 95%

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

et al. 2006

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Background: Intraventricular hemorrhage (IVH) is a major cause of neurologic disabilities in preterm newborns. We evaluated the use of plasma activin A concentrations to predict the development of perinatal IVH. Methods: We measured nucleated erythrocyte (NRBC) counts, plasma activin A, hypoxanthine (Hyp), and xanthine (Xan) in arterial blood samples obtained from 53 preterm infants during the first hour after birth. Cerebral ultrasound was performed within 48 h of birth and repeated at 5-or 6-day intervals until the age of 4 weeks. Results: Grade I or II IVH was detected during the first 10 days of life in 11 of 53 patients (21%). Activin A, Hyp, and Xan concentrations and NRBC counts were higher in preterm newborns who subsequently developed IVH than in those who did not (P <0.0001, except P ‫؍‬ 0.019 for Xan). Neonatal activin A was correlated (P <0.0001) with Hyp (r ‫؍‬ 0.95), Xan (r ‫؍‬ 0.90), and NRBC count (r ‫؍‬ 0.90) in newborns without later IVH and in those who developed IVH (Hyp, r ‫؍‬ 0.89, P ‫؍‬ 0.0002; Xan, r ‫؍‬ 0.95, P <0.0001; NRBC count, r ‫؍‬ 0.90, P ‫؍‬ 0.0002). At a cutoff of 0.8 g/L activin A, the sensitivity and specificity were 100% [11 of 11; 95% confidence interval (CI), 71%-100%] and 93% (39 of 42; 95% CI, 81%-98%), and positive and negative predictive values were 79% (95% CI, 61%-100%) and 0% (95% CI, 0%-2%), respectively. The area under the ROC curve was 0.98. Conclusions: Activin A concentrations at birth are increased in preterm newborns who later develop IVH

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Section: Discussionmentioning

confidence: 95%

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

et al. 2006

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“…Studies of activin expression patterns during decidualization in mice and rats have further suggested that activin expression may regulate decidual regression during placentation (22,63,64), and activin signaling is thought to regulate interactions between the fetal placenta and maternal decidua in humans (65,66); however, the roles of activin signaling in the decidua have not been well studied experimentally in vivo.…”

Section: (A) Expression Ofmentioning

confidence: 99%

Follistatin is critical for mouse uterine receptivity and decidualization

Fullerton

Monsivais

Kommagani

et al. 2017

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

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Embryo implantation remains a significant challenge for assisted reproductive technology, with implantation failure occurring in ∼50% of in vitro fertilization attempts. Understanding the molecular mechanisms underlying uterine receptivity will enable the development of new interventions and biomarkers. TGFβ family signaling in the uterus is critical for establishing and maintaining pregnancy. Follistatin (FST) regulates TGFβ family signaling by selectively binding TGFβ family ligands and sequestering them. In humans, FST is upregulated in the decidua during early pregnancy, and women with recurrent miscarriage have lower endometrial expression of FST during the luteal phase. Because global knockout of Fst is perinatal lethal in mice, we generated a conditional knockout (cKO) of Fst in the uterus using progesterone receptor-cre to study the roles of uterine Fst during pregnancy. Uterine Fst-cKO mice demonstrate severe fertility defects and deliver only 2% of the number of pups delivered by control females. In Fst-cKO mice, the uterine luminal epithelium does not respond properly to estrogen and progesterone signals and remains unreceptive to embryo attachment by continuing to proliferate and failing to differentiate. The uterine stroma of Fst-cKO mice also responds poorly to artificial decidualization, with lower levels of proliferation and differentiation. In the absence of uterine FST, activin B expression and signaling are up-regulated, and bone morphogenetic protein (BMP) signals are impaired. Our findings support a model in which repression of activin signaling by FST enables uterine receptivity by preserving critical BMP signaling.female infertility | implantation failure | TGFβ signaling | activin antagonism M ouse models are powerful tools for improving our understanding of uterine receptivity because mice can be easily manipulated with well-established genetic tools and experimental approaches (1). Studies using mice have shown that TGFβ family growth factors play critical roles in establishing uterine receptivity. The TGFβ family operates through a shared mechanism. The signaling cascade is initiated by binding of homodimeric or heterodimeric ligands to a cell-surface receptor complex composed of a type 2 receptor kinase and its partner type 1 receptor kinase. Once the ligand binds, the type 2 receptor phosphorylates and activates the type 1 receptor. The activated type 1 receptor kinase phosphorylates receptor SMADs, enabling them to form a complex with the co-SMAD, SMAD4. The resulting heterotrimeric SMAD complex concentrates in the nucleus where it regulates gene expression in conjunction with of a multitude of cofactors. Uterine conditional knockout (cKO) of TGFβ superfamily growth factors bone morphogenetic protein 2 (BMP2), type 1 receptors ALK2 and ALK3, and type 2 receptor bone morphogenetic protein receptor 2 (BMPR2) in mice have shown that local uterine TGFβ family signaling plays key roles in regulating embryo attachment and invasion as well as endometrial stromal cell decidualization (2-5)....

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“…Although the substrates for HtrA1 are yet to be identified, a recent study indicated that HtrA1 might be involved in regulating the TGF␤ signaling (Oka et al, 2004). Given that TGF␤ family members have been implicated in regulation of decidual regression during placental development (Moulton, 1994;Tessier et al, 2003), it is tempting to suggest that HtrA1 may exert its action in decidual involution in association with the TGF␤ signalling.…”

Section: Localization Of Htra1 Protein In the Uterus And Placentamentioning

confidence: 99%

“…Members of the transforming growth factor (TGF) ␤ family, including TGF␤1, TGF␤2 and activin have been implicated in regulation of decidual regression during placental development (Moulton, 1994;Tessier et al, 2003). In addition, apoptosis-associated factors, including sulfated glycoprotein-2, the caspase family proteases such as cathepsin-D, Bax, and Bcl2 have been shown to be associated with decidual regression (Gu et al, 1994;Moulton, 1994;Dai et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Serine protease HtrA1 is developmentally regulated in trophoblast and uterine decidual cells during placental formation in the mouse

Nie¹,

Li²,

Salamonsen³

2005

Developmental Dynamics

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Development of a hemochorial placenta involves trophoblast proliferation, differentiation, and invasion into the uterus to promote blood flow to the embryo. Trophoblast invasion is tightly controlled by expression of specific proteases in the trophoblast and highly coordinated activities in the uterus. One uterine event essential for placentation is the developmentally regulated formation and regression of the decidua. In mice, decidual regression takes place in a temporal-and spatial-specific manner that is coordinated with placental development. In this study, we identified that the serine protease HtrA1 (high temperature requirement factor A1) was specifically expressed in differentiated trophoblast cells, especially the giant cells, during the early stages of placental development. A high level of HtrA1 expression was also detected in decidua capsularis specifically at the decidual-trophoblast interface where active involution occurs. Thus, we have identified a previously unknown role for HtrA1 as a protease potentially important for trophoblast differentiation/invasion and uterine decidual regression during placental development.

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Decidual Activin: Its Role In the Apoptotic Process and Its Regulation by Prolactin1

Cited by 23 publications

References 41 publications

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

Follistatin is critical for mouse uterine receptivity and decidualization

Serine protease HtrA1 is developmentally regulated in trophoblast and uterine decidual cells during placental formation in the mouse

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