Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fetal and neonatal morbidity and mortality is high in severe pre-eclampsia compared with mild pre-eclampsia and normotensive pregnancies. Causes for these fetal disturbances had been associated with iatrogenic prematurity and reduction in placental blood flow. Actual evidences suggest that in severe (early-onset) pre-eclampsia a reduction in placental angiogenesis could be a mechanism responsible for the reduced placental blood flow, while in mild (late-onset) pre-eclampsia normal placental blood flow could result from either no alteration or increased placental angiogenesis, or reduced vessel resistance. Since adenosine is involved in endothelium proliferation and angiogenesis, and umbilical and maternal blood level of this nucleoside is elevated in pre-eclampsia compared with normal pregnancies, it is feasible that placental angiogenesis in mild and/or severe pre-eclampsia involves adenosine-dependent cell signaling mechanisms. There are not reports regarding adenosine role in placental angiogenesis neither in normal nor in pathological pregnancies. However, it is well established that adenosine stimulates adenosine receptors triggering expression of angiogenic factors such as vascular endothelial growth factor (VEGF). VEGF stimulates VEGF receptors type 1 and 2, activating signaling cascades that involve increased synthesis of endothelial-derived nitric oxide (NO). On the other hand, the soluble VEGF receptor type 1 (sFlt-1), whose plasma concentration is increased in severe compared with mild pre-eclampsia, reduces angiogenesis, spotting sFlt-1 as a factor that could potentially be involved in this phenomenon. This review focuses on the available evidence regarding a potential differential mechanism of placental angiogenesis in mild compared with severe pre-eclampsia, and analyzes the potential role of adenosine/VEGF/VEGF receptors/NO signaling cascade in this phenomenon.
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PMID:Potential cell signalling mechanisms involved in differential placental angiogenesis in mild and severe pre-eclampsia. 1948 94

CEACAM1 is the founder molecule of the family of 'carcinoembryonic antigen-related cell adhesion molecules' and part of the immunoglobulin superfamily. Due to its role as a coreceptor to many other receptors (e.g. Toll-like receptor 2, Toll-like receptor 4, T-cell receptor, B-cell receptor, epidermal growth factor receptor and vascular endothelial growth factor receptor) and its different isoforms, CEACAM1 is a multifunctional protein with an impact on proliferation and differentiation of multiple cell types. Although different modes of action in other tissues are described, the role of CEACAM1 in the developing brain remains elusive. Here we report for the first time that CEACAM1 is expressed ontogenetically in oligodendrocytes of the developing rat brain, and that CEACAM1 expression has a spatiotemporal relation to myelination. In addition, CEACAM1 expression is altered in a model of hyperoxia- and inflammation-induced encephalopathy of prematurity, a myelination disorder of children born preterm. Furthermore, primary oligodendrocytes stimulated with CEACAM1 show increased myelination. Therefore, we postulate that CEACAM1 is, at least in part, involved in hyperoxia- and inflammation-induced disruption of myelination, but may also play a role in intact myelination as it is ontogenetically expressed in myelinating oligodendrocytes.
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PMID:CEACAM1 expression in oligodendrocytes of the developing rat brain shows a spatiotemporal relation to myelination and is altered in a model of encephalopathy of prematurity. 2365 19