AI Article Synopsis
Article Abstract
Remodeling of uterine spiral arteries by trophoblast cells is a requisite process for hemochorial placentation and successful pregnancy. The rat exhibits deep intrauterine trophoblast invasion and accompanying trophoblast-directed vascular modification. The involvement of phosphatidylinositol 3 kinase (PI3K), AKT, and Fos-like antigen 1 (FOSL1) in regulating invasive trophoblast and hemochorial placentation was investigated using Rcho-1 trophoblast stem cells and rat models. Disruption of PI3K/AKT with small-molecule inhibitors interfered with the differentiation-dependent elaboration of a signature invasive-vascular remodeling trophoblast gene expression profile and trophoblast invasion. AKT isoform-specific knockdown also affected the signature invasive-vascular remodeling trophoblast gene expression profile. Nuclear FOSL1 increased during trophoblast cell differentiation in a PI3K/AKT-dependent manner. Knockdown of FOSL1 disrupted the expression of a subset of genes associated with the invasive-vascular remodeling trophoblast phenotype, including the matrix metallopeptidase 9 gene (Mmp9). FOSL1 was shown to occupy regions of the Mmp9 promoter in trophoblast cells critical for the regulation of Mmp9 gene expression. Inhibition of FOSL1 expression also abrogated trophoblast invasion, as assessed in vitro and following in vivo trophoblast-specific lentivirally delivered FOSL1 short hairpin RNA (shRNA). In summary, FOSL1 is a key downstream effector of the PI3K/AKT signaling pathway responsible for development of trophoblast lineages integral to establishing the maternal-fetal interface.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232930 | PMC |
| http://dx.doi.org/10.1128/MCB.05780-11 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
NETs exacerbate placental inflammation and injury through high mobility group protein B1 during preeclampsia.
Placenta
December 2024
Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China; Department of Clinical Laboratory, The Laboratory of Placenta-related Diseases, Key Laboratory of Birth Regulation and Control Technology of National Health and Family Planning Commission of China, Jinan, Shandong, 250014, China. Electronic address:
Background: Inflammatory stress at the maternal-fetal interface plays an important role in the occurrence and development of preeclampsia(PE) caused by different etiologies. Many pathological neutrophil extracellular traps (NETs) at the maternal-fetal interface are believed to be among the main pathogenic factors leading to preeclampsia and the worsening of its symptoms. However, the underlying mechanism is largely unclear.
View Article and Find Full Text PDFHuman Cytomegalovirus Replication Enhanced By Placental MicroRNAs.
J Med Virol
December 2024
Division of Microbiology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
Placental trophoblasts constitute the interface between the fetal and maternal environments and physically prevent maternal-fetal viral transmission. However, congenital human cytomegalovirus (HCMV) infection in the early stages of pregnancy results in severe symptoms in the fetus. HCMV is the most common causative agent of intrauterine infection.
View Article and Find Full Text PDFTwin pregnancies consisting of one normal fetus and one complete mole are very rare. The main concerning risks associated with the continuation of such pregnancy are hyperthyroidism, theca lutein cysts, preeclampsia, and the development of GTD (gestational trophoblastic disease) spectrum (neoplasia) in the mother, which is due to high human chorionic gonadotropin (HCG) values, and intrauterine death and prematurity in the coexistent normal fetus. We report the successful outcome of conservative management in a healthy mother and baby.
View Article and Find Full Text PDFAn update review of the application of single-cell RNA sequencing in pregnancy-related diseases.
Front Endocrinol (Lausanne)
December 2024
Department of Obstetrics, The First Hospital of China Medical University, Shenyang, China.
Reproductive success hinges on the presence of a robust and functional placenta. Examining the placenta provides insight about the progression of pregnancy and valuable information about the normal developmental trajectory of the fetus. The current limitations of using bulk RNA-sequencing (RNA-seq) analysis stem from the diverse composition of the placenta, hindering a comprehensive description of how distinct trophoblast cell expression patterns contribute to the establishment and sustenance of a successful pregnancy.
View Article and Find Full Text PDFDHA Improves neurodevelopmental abnormalities in offspring of gestational diabetes mellitus patients via the PPAR-γ/FATP4 pathway.
Biochem Pharmacol
December 2024
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; National Clinical Research Center for Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Offspring of women with gestational diabetes mellitus (GDM) face an increased risk of long-term neurodevelopmental abnormalities. This study explores the altered expression of key placental fatty acid transport proteins-FATP2, FATP4, FATP6, FABP4, and FAT/CD36-in GDM patients, and the potential of docosahexaenoic acid (DHA) to mitigate neurodevelopmental risks in offspring by enhancing their expression through activation of peroxisome proliferator-activated receptor γ (PPAR-γ). Our findings demonstrate that placental FATP4 expression is reduced in GDM patients.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!