Histologic Evidence of Epithelial–Mesenchymal Transition and Autophagy in Human Fetal Membranes

Severino, Mary E.; Richardson, Lauren S.; Kacerovsky, Marian; Menon, Ramkumar

doi:10.1016/j.ajpath.2023.12.011

Cited by 4 publications

(2 citation statements)

References 62 publications

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“…In this research, we discovered that almost all extracted primary cells could express CK18, but not vimentin, indicating that the separated cells were epithelial cells and have not transformed into mesenchymal cells. CK18 was an epithelial cell marker, which has been used to identify epithelial cells . Vimentin was a mesenchymal cell marker, which has also been used to identify epithelial cells .…”

Section: Discussionmentioning

confidence: 99%

Bta-miR-200a Regulates Milk Fat Biosynthesis by Targeting IRS2 to Inhibit the PI3K/Akt Signal Pathway in Bovine Mammary Epithelial Cells

Tan,

Yang,

Qiu

et al. 2024

J. Agric. Food Chem.

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Milk fat synthesis has garnered significant attention due to its influence on the quality of milk. Recently, an increasing amount of proofs have elucidated that microRNAs (miRNAs) are important post-transcriptional factor involved in regulating gene expression and play a significant role in milk fat synthesis. MiR-200a was differentially expressed in the mammary gland tissue of dairy cows during different lactation periods, which indicated that miR-200a was a candidate miRNA involved in regulating milk fat synthesis. In our research, we investigated the potential function of miR-200a in regulating milk fat biosynthesis in bovine mammary epithelial cells (BMECs). We discovered that miR-200a inhibited cellular triacylglycerol (TAG) synthesis and suppressed lipid droplet formation; at the same time, miR-200a overexpression suppressed the mRNA and protein expression of milk fat metabolismrelated genes, such as fatty acid synthase (FASN), peroxisome proliferator-activated receptor gamma (PPARγ), sterol regulatory element-binding protein 1 (SREBP1), CCAAT enhancer binding protein alpha (CEBPα), etc. However, knocking down miR-200a displayed the opposite results. We uncovered that insulin receptor substrate 2 (IRS2) was a candidate target gene of miR-200a through the bioinformatics online program TargetScan. Subsequently, it was confirmed that miR-200a directly targeted the 3′untranslated region (3′-UTR) of IRS2 via real-time fluorescence quantitative PCR (RT-qPCR), western blot analysis, and dualluciferase reporter gene assay. Additionally, IRS2 knockdown in BMECs has similar effects to miR-200a overexpression. Our research set up the mechanism by which miR-200a interacted with IRS2 and discovered that miR-200a targeted IRS2 and modulated the activity of the PI3K/Akt signaling pathway, thereby taking part in regulating milk fat synthesis in BMECs. Our research results provided valuable information on the molecular mechanisms for enhancing milk quality from the view of miRNA-mRNA regulatory networks.

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Section: Discussionmentioning

confidence: 99%

Bta-miR-200a Regulates Milk Fat Biosynthesis by Targeting IRS2 to Inhibit the PI3K/Akt Signal Pathway in Bovine Mammary Epithelial Cells

Tan,

Yang,

Qiu

et al. 2024

J. Agric. Food Chem.

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“…PROM before 37 weeks of gestation occurs in around 3% of all pregnancies, was significantly associated with more severe perinatal complications such as premature delivery, chorioamnionitis, and placental abruption, and is the main cause of maternal perinatal death [ 3 , 4 ]. It is generally accepted that PROM is a multifactorial disease with multiple causes (e.g., infection and endocrine disruption) [ 5 , 6 ], and the biological changes of membranes are the core pathological basis of PROM, including matrix degradation, cell senescence, apoptosis, autophagy, and epithelial–mesenchymal transition [ 7 , 8 ]. However, as the most common perinatal disease, research on PROM often focused on the prediction of severe maternal–fetal outcomes via common biomarkers [ 9 , 10 ], and the core etiology and key molecular mechanism of PROM remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Identification of circRNA Expression Profile and Potential Systemic Immune Imbalance Modulation in Premature Rupture of Membranes

Huang,

Ran,

Chen

et al. 2024

Analytical Cellular Pathology

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Premature rupture of membrane (PROM) refers to the rupture of membranes before the onset of labor which increases the risk of perinatal morbidity and mortality. Recently, circular RNAs (circRNAs) have emerged as promising regulators of diverse diseases. However, the circRNA expression profiles and potential circRNA–miRNA–mRNA regulatory mechanisms in PROM remain enigmatic. In this study, we displayed the expression profiles of circRNAs and mRNAs in plasma and fetal membranes of PROM and normal control (NC) groups based on circRNA microarray, the Gene Expression Omnibus database, and NCBI’s Sequence Read Archive. A total of 1,459 differentially expressed circRNAs (DECs) in PROM were identified, with 406 upregulated and 1,053 downregulated. Then, we constructed the circRNA–miRNA–mRNA network in PROM, encompassing 22 circRNA–miRNA pairs and 128 miRNA–mRNA pairs. Based on the analysis of gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene set enrichment analysis (GSEA), DECs were implicated in immune-related pathways, with certain alterations persisting even postpartum. Notably, 11 host genes shared by DECs of fetal membrane tissue and prenatal plasma in PROM were significantly implicated in inflammatory processes and extracellular matrix regulation. Our results suggest that structurally stable circRNAs may predispose to PROM by mediating systemic immune imbalances, including peripheral leukocyte disorganization, local immune imbalance at the maternal–fetal interface, and local collagen disruption. This is the first time to decipher a landscape on circRNAs of PROM, reveals the pathogenic cause of PROM from the perspective of circRNA, and opens up a new direction for the diagnosis and treatment of PROM.

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Lead exposure at the feto-maternal interface: a cause for concern for fetal membrane trophoblasts

Flores-Espinosa,

Menon,

Kammala

et al. 2024

Toxicological Sciences

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The integrity of fetal membranes enables biological functions that protect the fetus and maintain the pregnancy. Any compromise in fetal membrane function can predispose a pregnant woman to prelabor rupture of the membranes (pPROM) and subsequently to preterm birth (PTB). Epidemiologic data suggest that lead exposure during pregnancy is one of several risk factors associated with PTB and pPROM. This heavy metal can cross placental and fetal membrane barriers, disrupting homeostasis in these tissues. Autophagy contributes to the maintenance of fetal membrane homeostasis during gestation, and dysfunctional autophagy is associated with pPROM. In this study, we determined the mechanistic impact of lead-induced cellular changes, autophagy, senescence, and inflammation in chorion trophoblast cells (CTCs) and amnion epithelial cells (AECs) of the fetal membranes. Lead exposure in CTCs induced autophagy disfunction (increase in LC3B-II), augmented senescence (increased SA-β-galactosidase activity) and increased the release of inflammation. In AECs, lead exposure did effect autophagy, senescence, nor inflammation. The differential changes observed in CTCs and AECs after exposure to high lead concentrations may promote the weakening of fetal membranes and contribute to preterm rupture.

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Histologic Evidence of Epithelial–Mesenchymal Transition and Autophagy in Human Fetal Membranes

Cited by 4 publications

References 62 publications

Bta-miR-200a Regulates Milk Fat Biosynthesis by Targeting IRS2 to Inhibit the PI3K/Akt Signal Pathway in Bovine Mammary Epithelial Cells

Bta-miR-200a Regulates Milk Fat Biosynthesis by Targeting IRS2 to Inhibit the PI3K/Akt Signal Pathway in Bovine Mammary Epithelial Cells

Identification of circRNA Expression Profile and Potential Systemic Immune Imbalance Modulation in Premature Rupture of Membranes

Lead exposure at the feto-maternal interface: a cause for concern for fetal membrane trophoblasts

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