Insights into the mechanism of CXCL12-mediated signaling in trophoblast functions and placental angiogenesis
Autor: | Tao Han, Liang Wang, Wen-li Gou, Yingli Lian, Xueyi Li, Xiaoming Zhu, Chao Fang, Yilin Zhao |
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Rok vydání: | 2015 |
Předmět: |
medicine.medical_specialty
Spiral artery Stromal cell Angiogenesis Placenta Biophysics Neovascularization Physiologic Biology Biochemistry Pregnancy Internal medicine medicine Humans Decidual cells reproductive and urinary physiology Orphan receptor Placentation Trophoblast General Medicine Chemokine CXCL12 biological factors Trophoblasts Cell biology Endocrinology medicine.anatomical_structure embryonic structures Female biological phenomena cell phenomena and immunity Signal Transduction |
Zdroj: | Acta Biochimica et Biophysica Sinica. 47:663-672 |
ISSN: | 1672-9145 |
DOI: | 10.1093/abbs/gmv064 |
Popis: | The chemokine CXCL12 and its receptor CXCR4 are important signaling components required for human blastocyst implantation and the progression of pregnancy. Growing evidence indicates that the CXCL12/CXCR4 axis can regulate trophoblast function and uterine spiral artery remodeling, which plays a fundamental role in placentation and fetal outcome. The orphan receptor CXCR7 is also believed to partly regulate the function of the CXCL12/CXCR4 axis. Additionally, the CXCL12/CXCR4/CXCR7 axis can enhance the cross-talk between trophoblasts and decidual cells such as uterine natural killer cells and decidual stromal cells which are involved in regulation of trophoblast differentiation and invasion and placental angiogenesis. In addition, recent studies proved that CXCL12 expression is elevated in the placenta and mid-trimester amniotic fluid of pregnant women with preeclampsia, implying that dysregulation of CXCL12 plays a role in the pathogenesis of preeclampsia. Further understanding of the regulatory mechanisms of CXCL12-mediated signaling in trophoblast functions and placental angiogenesis may help to design novel therapeutic approaches for pregnancy-associated diseases. |
Databáze: | OpenAIRE |
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