Syncytiotrophoblast of Placentae from Women with Zika Virus Infection Has Altered Tight Junction Protein Expression and Increased Paracellular Permeability

Miranda, Jael; Martín-Tapia, Dolores; Valdespino-Vázquez, Yolotzin; Alarcón, Lourdes; Espejel-Núñez, Aurora; Guzmán-Huerta, Mario; Muñoz-Medina, José Esteban; Shibayama, Mineko; Chávez‐Munguía, Bibiana; Estrada-Gutiérrez, Guadalupe; Liévano, Samuel; Ludert, Juan E.; González‐Mariscal, Lorenza

doi:10.3390/cells8101174

Cited by 50 publications

(41 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Histological evaluations of the placenta and umbilical cord shed further light on the maternal‐fetal response to viral infections 28 . Placental trophoblastic apoptosis and vascular damage contribute to increased permeability of the placenta 118 . In SARS‐CoV‐1, during the acute phase, maternal hypoxia may have caused maternal placental blood flow disturbances leading to increased subchorionic or intervillous fibrin deposition; whilst during the convalescent phase, extensive fetal thrombotic vasculopathy with avascular fibrotic villi was observed.…”

Section: What Do We Know About Mother‐to‐child‐transmission Of Sars‐cmentioning

confidence: 99%

Mechanisms and evidence of vertical transmission of infections in pregnancy including SARS‐CoV‐2s

et al. 2020

View full text Add to dashboard Cite

There remain unanswered questions concerning mother-to-child-transmission of SARS-CoV-2. Despite reports of neonatal COVID-19, SARS-CoV-2 has not been consistently isolated in perinatal samples, thus definitive proof of transplacental infection is still lacking. To address these questions, we assessed investigative tools used to confirm maternal-fetal infection and known protective mechanisms of the placental barrier that prevent transplacental pathogen migration. Forty studies of COVID-19 pregnancies reviewed suggest a lack of consensus on diagnostic strategy for congenital infection. Although real-time polymerase chain reaction of neonatal swabs was universally performed, a wide range of clinical samples was screened including vaginal secretions (22.5%), amniotic fluid (35%), breast milk (22.5%) and umbilical cord blood. Neonatal COVID-19 was reported in eight studies, two of which were based on the detection of SARS-CoV-2 IgM in neonatal blood. Histological examination demonstrated sparse viral particles, vascular malperfusion and inflammation in the placenta from pregnant women with COVID-19. The paucity of placental coexpression of ACE-2 and TMPRSS2, two receptors involved in cytoplasmic entry of SARS-CoV-2, may explain its relative insensitivity to transplacental infection. Viral interactions may utilise membrane receptors other than ACE-2 thus, tissue susceptibility may be broader than currently known. Further spatial-temporal studies are needed to determine the true potential for transplacental migration.

show abstract

Section: What Do We Know About Mother‐to‐child‐transmission Of Sars‐cmentioning

confidence: 99%

Mechanisms and evidence of vertical transmission of infections in pregnancy including SARS‐CoV‐2s

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The permeability of the TJ present in the superficial cells of the multi-stratified epithelium of the cervix of mice was evaluated using the paracellular pathway marker ruthenium red, as previously reported (34,35). Thus, if the ruthenium red stain only highlighted the apical surface of the superficial cells in the cervix, this indicated that passage through the paracellular pathway was blocked due to TJ sealing.…”

Section: Transmission Electron Microscopy (Tem)mentioning

confidence: 95%

E7 oncoprotein from human papillomavirus 16 alters claudins expression and the sealing of epithelial tight junctions

Uc¹,

Miranda²,

Raya‐Sandino³

et al. 2020

Int J Oncol

Self Cite

View full text Add to dashboard Cite

Tight junctions (TJs) are cell-cell adhesion structures frequently altered by oncogenic transformation. In the present study the role of human papillomavirus (HPV) 16 E7 oncoprotein on the sealing of TJs was investigated and also the expression level of claudins in mouse cervix and in epithelial Madin-Darby Canine Kidney (MDCK) cells. It was found that there was reduced expression of claudins-1 and-10 in the cervix of 7-month-old transgenic K14E7 mice treated with 17β-estradiol (E 2), with invasive cancer. In addition, there was also a transient increase in claudin-1 expression in the cervix of 2-month-old K14E7 mice, and claudin-10 accumulated at the border of cells in the upper layer of the cervix in FvB mice treated with E 2 , and in K14E7 mice treated with or without E 2. These changes were accompanied by an augmented paracellular permeability of the cervix in 2-and 7-month-old FvB mice treated with E 2 , which became more pronounced in K14E7 mice treated with or without E 2. In MDCK cells the stable expression of E7 increased the space between adjacent cells and altered the architecture of the monolayers, induced the development of an acute peak of transepithelial electrical resistance accompanied by a reduced expression of claudins-1,-2 and-10, and an increase in claudin-4. Moreover, E7 enhances the ability of MDCK cells to migrate through a 3D matrix and induces cell stiffening and stress fiber formation. These observations revealed that cell transformation induced by HPV16 E7 oncoprotein was accompanied by changes in the pattern of expression of claudins and the degree of sealing of epithelial TJs.

show abstract

“…Despite some knowledge regarding ZIKV pathogenesis, its mechanism of infection in placental immune cell types remains limited (116)(117)(118)(119). Histopathology of ZIKV infected placentae has shown ZIKV infection in first trimester villous stromal tissue cells, which includes immune cells in the chorionic villi (117,120,121). Uniquely, ZIKV was also found to infect CTBs, endothelial cells, fibroblasts and HC in chorionic villi, as well as amniotic epithelial cells and trophoblast progenitor cells (103,(116)(117)(118)(122)(123)(124) (Figure 4).…”

Section: Zikvmentioning

confidence: 99%

Viral-Immune Cell Interactions at the Maternal-Fetal Interface in Human Pregnancy

et al. 2020

View full text Add to dashboard Cite

The human decidua and placenta form a distinct environment distinguished for its promotion of immunotolerance to infiltrating semiallogeneic trophoblast cells to enable successful pregnancy. The maternal-fetal interface also successfully precludes transmission of most pathogens. This barrier function occurs in conjunction with a diverse influx of decidual immune cells including natural killer cells, macrophages and T cells. However, several viruses, among other microorganisms, manage to escape destruction by the host adaptive and innate immune system, leading to congenital infection and adverse pregnancy outcomes. In this review, we describe mechanisms of pathogenicity of two such viral pathogens, Human cytomegalovirus (HCMV) and Zika virus (ZIKV) at the maternal-fetal interface. Host decidual immune cell responses to these specific pathogens will be considered, along with their interactions with other cell types and the ways in which these immune cells may both facilitate and limit infection at different stages of pregnancy. Neither HCMV nor ZIKV naturally infect commonly used animal models [e.g., mice] which makes it challenging to understand disease pathogenesis. Here, we will highlight new approaches using placenta-on-a-chip and organoids models that are providing functional and physiologically relevant ways to study viral-host interaction at the maternal-fetal interface.

show abstract

Syncytiotrophoblast of Placentae from Women with Zika Virus Infection Has Altered Tight Junction Protein Expression and Increased Paracellular Permeability

Cited by 50 publications

References 68 publications

Mechanisms and evidence of vertical transmission of infections in pregnancy including SARS‐CoV‐2s

Mechanisms and evidence of vertical transmission of infections in pregnancy including SARS‐CoV‐2s

E7 oncoprotein from human papillomavirus 16 alters claudins expression and the sealing of epithelial tight junctions

Viral-Immune Cell Interactions at the Maternal-Fetal Interface in Human Pregnancy

Contact Info

Product

Resources

About