placental insufficiency/protease

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The channel-activating protease CAP1/Prss8 is required for placental labyrinth maturation.

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The serine protease CAP1/Prss8 is crucial for skin barrier function, lung alveolar fluid clearance and has been unveiled as diagnostic marker for specific cancer types. Here, we show that a constitutive knockout of CAP1/Prss8 leads to embryonic lethality. These embryos presented no specific defects,

Serum insulin-like growth factor-binding protein-3 (IGFBP-3) levels and IGFBP-3 protease activity in normal, abnormal, and multiple human pregnancy.

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Proteolytic activity directed against insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) is found in human pregnancy serum. We have investigated changes in this protease activity in pregnancies in which the fetus is small for gestational age and in multiple pregnancies. Maternal serum was

Extraembryonic but not embryonic SUMO-specific protease 2 is required for heart development.

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SUMO-specific protease 2 (SENP2) activities to remove SUMO from its substrates is essential for development of trophoblast stem cells, niches and lineages. Global deletion of SENP2 leads to midgestation lethality, and causes severe defects in the placenta which is accompanied by embryonic brain and

TCDD induces the hypoxia-inducible factor (HIF)-1α regulatory pathway in human trophoblastic JAR cells.

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The exposure to dioxin can compromise pregnancy outcomes and increase the risk of preterm births. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been demonstrated to induce placental hypoxia at the end of pregnancy in a rat model, and hypoxia has been suggested to be the cause of abnormal

Decidual-secreted factors alter invasive trophoblast membrane and secreted proteins implying a role for decidual cell regulation of placentation.

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Inadequate or inappropriate implantation and placentation during the establishment of human pregnancy is thought to lead to first trimester miscarriage, placental insufficiency and other obstetric complications. To create the placental blood supply, specialized cells, the 'extravillous trophoblast'

Clinical Importance of Low Level of PAPP-A in First Trimester of Pregnancy - An Obstetrical Dilemma in Chromosomally Normal Fetus.

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A variety of recent evidence exists about the clinical implication of low level of Pregnancy-associated plasma protein A (PAPP-A) in pregnancy. This glycoprotein is a protease, which releases the Insulin-like growth factor from IGFBP 4. Its role is a trophoblastic invasion of decidua,

The Reactivity Levels of Progesterone, Nitric Oxide and Nuclear Factor Kappa-B on the Serum of Term and Post-Term Pregnancy, Clinical Study in Padang, West Sumatera, Indonesia.

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The requirement of SUMO2/3 for SENP2 mediated extraembryonic and embryonic development.

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SUMO-specific protease 2 (SENP2) is essential for the development of healthy placenta. The loss of SENP2 causes severe placental deficiencies and leads to embryonic death that is associated with heart and brain deformities. However, tissue-specific disruption of SENP2 demonstrates its dispensable

Blood serum characteristics of newborn pigs: comparison of unaffected pigs with pigs belonging to five mortality groups.

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The blood serum levels of glucose, hemoglobin, insulin, cortisol, albumin, alpha-fetoprotein, alpha 2-macroglobulin f and s, alpha 2-antitrypsin inhibitor and alpha 1-protease inhibitor were determined at birth in 5 clinically and morphologically identified mortality groups of pigs. These were

IGFBP-4 and -5 are expressed in first-trimester villi and differentially regulate the migration of HTR-8/SVneo cells.

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BACKGROUND Adverse gestational outcomes such as preeclampsia (PE) and intrauterine growth restriction (IUGR) are associated with placental insufficiency. Normal placental development relies on the insulin-like growth factors -I and -II (IGF-I and -II), in part to stimulate trophoblast proliferation

Maternal HtrA3 optimizes placental development to influence offspring birth weight and subsequent white fat gain in adulthood.

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High temperature requirement factor A3 (HtrA3), a member of the HtrA protease family, is highly expressed in the developing placenta, including the maternal decidual cells in both mice and humans. In this study we deleted the HtrA3 gene in the mouse and crossed females carrying zero, one, or two

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