Cross talk: Trafficking and functional impact of maternal exosomes at the Feto-maternal Interface under normal and pathologic states

2021 ◽  
Author(s):  
Ourlad Alzeus G Tantengco ◽  
Enkhtuya Radnaa ◽  
Hend Shahin ◽  
Talar Kechichian ◽  
Ramkumar Menon
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Inflammatory Status ◽  
Decidual Cells ◽  
Cytokine Levels ◽  
Cargo Proteins ◽  
Cervical Cells ◽  
And Oxidative Stress ◽  
Amnion Epithelial Cells ◽  
Pro Inflammatory Cytokines

Abstract Fetal cell-derived exosomes promote inflammation in uterine and cervical cells to promote labor and delivery. However, the effect of maternal exosomes on fetal cells is still not known. We tested the hypothesis that cervical cells exposed to infectious and oxidative stress (OS) signals produce exosomes that can induce inflammation at the feto-maternal interface (FMi). Exosomes isolated from medium samples from human ectocervical epithelial cells (Ecto), endocervical epithelial cells (Endo), and cervical stromal cells (Stroma) in normal cell culture (control) or exposed to infection or OS conditions were characterized based on morphology, size, quantity, expression of tetraspanin markers, and cargo proteins. Human decidual, chorion trophoblast (CTC), chorion mesenchymal (CMC), amnion mesenchymal (AMC), and amnion epithelial cells (AEC) were treated with control, LPS-, or OS-treated cervical exosomes. ELISA for pro-inflammatory cytokines and progesterone was done to determine the recipient cells’ inflammatory status. Ecto, endo, and stroma released ∼110 nm, cup-shaped exosomes. LPS and OS treatments did not affect exosome size; however, OS significantly increased the number of exosomes released by all cervical cells. Cervical exosomes were detected by fluorescence microscopy in each target cell after treatment. Exosomes from LPS- and CSE-treated cervical cells increased the inflammatory cytokine levels in the decidual cells, CMC, AMC, and AEC. LPS-treated stromal cell exosomes increased IL-6, IL-8, and progesterone in CTC. In conclusion, infection and OS can produce inflammatory cargo-enriched cervical exosomes that can destabilize FMi cells. However, the refractoriness of CTC to exosome treatments suggests a barrier function of the chorion at the FMi.

scholarly journals A distinct mechanism of senescence activation in amnion epithelial cells by infection, inflammation, and oxidative stress

2017 ◽  
Vol 79 (3) ◽  
pp. e12790 ◽  
Author(s):  
Christopher Luke Dixon ◽  
Lauren Richardson ◽  
Samantha Sheller-Miller ◽  
George Saade ◽  
Ramkumar Menon
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Distinct Mechanism ◽  
And Oxidative Stress ◽  
Amnion Epithelial Cells

scholarly journals The Extent to which Relaxin Promotes Proliferation and Inhibits Apoptosis of Cervical Epithelial and Stromal Cells Is Greatest during Late Pregnancy in Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 511-518 ◽  
Author(s):  
Hyung-Yul Lee ◽  
Shuangping Zhao ◽  
P. A. Fields ◽  
O. D. Sherwood
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
Epithelial Cells ◽  
Stromal Cells ◽  
Late Pregnancy ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Apoptotic Cells ◽  
Cervical Cells

Relaxin promotes marked growth of the cervix during the second half of rat pregnancy, and this growth is accompanied by an increase in both epithelial and stromal cells. The objective of this study was to test the hypothesis that the extent to which relaxin promotes proliferation and inhibits apoptosis of cervical cells is greatest during late pregnancy in rats. The influence of neutralization of circulating relaxin by iv injection of 5 mg monoclonal antibody against rat relaxin (MCA1) was examined at 3-d intervals throughout the second half of pregnancy. Controls were injected with either 5 mg monoclonal antibody against fluorescein or 0.5 ml PBS vehicle. To evaluate cell proliferation, 5′-bromo-2-deoxyuridine was injected sc 8 h before cervixes were collected. Terminal deoxynucleotidyl transferase-mediated deoxyuridine 5′-triphosphate nick end-labeling and electron microscopy were used to detect apoptotic cells. Neutralization of relaxin with MCA1 decreased the rate of proliferation and increased the rate of apoptosis of cervical cells by d 13. However, the extent to which relaxin influenced these processes was greatest and dramatic by late pregnancy. In MCA1-treated rats on d 22 of pregnancy, the rates of proliferation of both epithelial and stromal cells were less than 20% those in controls, and the rates of apoptosis in epithelial cells and stromal cells were more than 10- and 3-fold, respectively, greater than those in controls. In conclusion, this study provides evidence that the extent to which relaxin promotes proliferation and inhibits apoptosis of cervical epithelial and stromal cells is greatest during late pregnancy.

scholarly journals Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 295 ◽  
Author(s):  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Ming-Chin Yu ◽  
Kuo-Wei Yeh ◽  
Szu-Chuan Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Lavage Fluid ◽  
Eosinophil Infiltration ◽  
Sesame Seeds ◽  
Cytokine Levels ◽  
And Oxidative Stress

Sesamol, isolated from sesame seeds (Sesamum indicum), was previously shown to have antioxidative, anti-inflammatory, and anti-tumor effects. Sesamol also inhibited lipopolysaccharide (LPS)-induced pulmonary inflammatory response in rats. However, it remains unclear how sesamol regulates airway inflammation and oxidative stress in asthmatic mice. This study aimed to investigate the efficacy of sesamol on oxidative stress and airway inflammation in asthmatic mice and tracheal epithelial cells. BALB/c mice were sensitized with ovalbumin, and received oral sesamol on days 14 to 27. Furthermore, BEAS-2B human bronchial epithelial cells were treated with sesamol to investigate inflammatory cytokine levels and oxidative responses in vitro. Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung, airway hyperresponsiveness, and T helper 2 cell-associated (Th2) cytokine expressions in bronchoalveolar lavage fluid and the lungs. Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice. We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells. Moreover, sesamol alleviated reactive oxygen species formation, and suppressed intercellular cell adhesion molecule-1 (ICAM-1) expression, which reduced monocyte cell adherence. We demonstrated that sesamol showed potential as a therapeutic agent for improving asthma.

Oxidative stress promotes cellular damages in the cervix: implications for normal and pathologic cervical function in human pregnancy

2021 ◽  
Author(s):  
Ourlad Alzeus G Tantengco ◽  
Joy Vink ◽  
Paul Mark B Medina ◽  
Ramkumar Menon
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Epithelial Cells ◽  
Cell Fate ◽  
Stromal Cells ◽  
Sterile Inflammation ◽  
Cellular Damage ◽  
Cervical Ripening ◽  
Pathway Activation ◽  
Cervical Cells

Abstract A physiologic increase in reactive oxygen species (ROS) throughout pregnancy is required to remodel the cervix. Oxidative stress (OS) can cause cellular damage that contributes to dysfunctional tissue. This study determined the effects of OS and the OS-induced cell fate of human cervical epithelial and cervical stromal cells. We treated the ectocervical and endocervical epithelial cells and cervical stromal cells with cigarette smoke extract (CSE), an OS inducer, for 48 h. Cell viability (crystal violet assay); cell cycle, apoptosis and necrosis (flow cytometry); senescence (senescence-associated β-galactosidase staining); autophagy (staining for autophagosome protein LC3B); stress signaler p38MAPK pathway activation (Western blot analyses); and inflammation by measuring IL-6 (ELISA) were conducted after 48 h of CSE treatment. OS induced ROS production in cervical cells, which was inhibited by the antioxidant N-acetylcysteine. OS promoted cell cycle arrest, induced necrosis but not apoptosis in cervical cells. High senescence and low autophagy were observed in cervical stromal cells under OS. Conversely, senescence was low and autophagy was high in endocervical epithelial cells. OS induced p38MAPK activation in all three cervical cells but only increased IL-6 production by the ectocervical epithelial cells. Inhibition of IL-6 production by a p38MAPK inhibitor confirmed activation of an OS-induced pathway. In conclusion, OS can promote different forms of cell death and sterile inflammation that is likely mediated by p38MAPK activation in the cellular components of the cervix. These OS-mediated cellular damages may contribute to the normal and premature cervical ripening process, which can predispose patients to preterm birth.

scholarly journals Cyclin D3 in the mouse uterus is associated with the decidualization process during early pregnancy

1999 ◽  
Vol 22 (1) ◽  
pp. 91-101 ◽  
Author(s):  
SK Das ◽  
H Lim ◽  
BC Paria ◽  
SK Dey
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Cyclin D3 ◽  
Northern Hybridization ◽  
Decidual Cell ◽  
Cell Reaction ◽  
Mouse Uterus ◽  
Decidual Cells ◽  
A Cell ◽  
Hybridization In Situ

In the mouse, the attachment reaction between the blastocyst trophectoderm and the receptive uterine luminal epithelium occurs at 2200-2300 h on day 4 of pregnancy and is rapidly followed by transformation of stromal cells into decidual cells (decidual cell reaction). This process can also be induced experimentally (deciduoma) by intraluminal oil infusion in the uterus on day 4 of pseudopregnancy. The decidual cell reaction is associated with up- and down-regulation of many genes in a cell-specific manner. Using mRNA differential display, we identified cyclin D3 as one of the genes that is upregulated in the uterus at the sites of blastocyst apposition during the attachment reaction. The levels of expression were low in the morning of days 1-4 as determined by Northern hybridization. In situ hybridization analysis showed that on days 1 and 2, signals were primarily localized in uterine epithelial cells, while signals were detected in both the stromal and epithelial cells on days 3 and 4. In contrast, with the initiation and progression of decidualization on days 5, 6 and 7, the levels of cyclin D3 mRNA were remarkably upregulated in stromal cells both at the mesometrial and the antimesometrial poles. However, on day 8, signals were primarily localized in stromal cells at the mesometrial decidual bed. Implanting blastocysts on these days also expressed cyclin D3 mRNA. In the progesterone-treated delayed implanting mice, the uterine levels of cyclin D3 mRNA were modest at the sites of blastocyst apposition, but were upregulated with the onset of implantation by estradiol-17beta. However, the decidual expression of cyclin D3 mRNA was not dependent on the presence of blastocysts, since increased expression also occurred in experimentally induced deciduoma in the absence of blastocysts. The importance of cyclin D3 in decidualization was further examined in Hoxa-10-deficient mice which show defective decidualization. The expression of cyclin D3 mRNA in Hoxa-10(-/-) uteri on day 5 was severely compromised after application of a deciduogenic stimulus on day 4 of pseudopregnancy. Collectively, the results suggest that cyclin D3 could be important for the process of decidualization.

Time Series Analysis of Transmesothelial Invasion by Endometrial Stromal and Epithelial Cells Using Three-dimensional Confocal Microscopy

2001 ◽  
Vol 7 (S2) ◽  
pp. 580-581
Author(s):  
CA Witz ◽  
S Cho ◽  
VE Centonze ◽  
IA Montoya-Rodriguez ◽  
RS Schenken
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Time Course ◽  
Three Dimensional ◽  
Collagen Iv ◽  
Mesothelial Cells ◽  
Endometrial Stromal Cells ◽  
Human Collagen ◽  
Endometrial Epithelial Cells

Using human peritoneal explants, we have previously demonstrated that endometrial stromal cells (ESCs) and endometrial epithelial cells (EECs) attach to intact mesothelium. Attachment occurs within one hour and mesothelial invasion occurs within 18 hours (Figure 1). We have also demonstrated that, in vivo, the mesothelium overlies a continuous layer of collagen IV (Col IV).More recently we have used CLSM, to study the mechanism and time course of ESC and EEC attachment and invasion through mesothelial monolayers. in these studies, CellTracker® dyes were used to label cells. Mesothelial cells were labeled with chloromethylbenzoylaminotetramethylrhodamine (CellTracker Orange). Mesothelial cells were then plated on human collagen IV coated, laser etched coverslips. Mesothelial cells were cultured to subconfluence. ESCs and EECs, labeled with chloromethylfluorscein diacetate (CellTracker Green) were plated on the mesothelial monolayers. Cultures were examined at 1, 6, 12 and 24 hours with simultaneous differential interference contrast and CLSM.

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

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