Endovascular trophoblast and spiral artery remodeling

Sato, Yukiyasu

doi:10.1016/j.mce.2019.110699

Cited by 82 publications

(57 citation statements)

References 51 publications

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“…Differences in the methods of tissue sampling, cell isolation and inefficiencies in detection of lowabundance transcripts in scRNA-seq can underestimate the actual frequencies of ACE2 + cells in a given tissue. Indeed, the dataset used in this study is exclusively of MACS enriched trophoblast preparations while the datasets used by Pique-Regi et al (2019, 2020 are a mixed population of cells from the feto-maternal interface. It is known that fractionated cell preparations allow better identification of low abundance transcripts in rare cell populations (Nguyen et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…While both these EVTs are invasive in nature, they have differential expression of certain marker genes. For example, endovascular EVTs overexpress the CDH5 and VCAM, they also have higher expression of CCR1 and CD59 (Bulla et al, 2005;Cartwright and Balarajah, 2005;Liu et al, 2018;Ueda et al, 2019;Sato, 2020). Intriguingly, the ACE2 + TMPRSS2 + cells also overexpressed several of the key endovascular EVT markers including CDH5, CCD5, CD59, and VCAM, indicating that the ACE2 + TMPRSS2 + population of second trimester EVTs are potentially endovascular trophoblasts and are targets of SARS-CoV-2 infection.…”

Section: Discussionmentioning

confidence: 99%

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Single-Cell RNA-seq Identifies Cell Subsets in Human Placenta That Highly Expresses Factors Driving Pathogenesis of SARS-CoV-2

Ashary

Bhide

Chakraborty

et al. 2020

Front. Cell Dev. Biol.

109

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Single-Cell RNA-seq Identifies Cell Subsets in Human Placenta That Highly Expresses Factors Driving Pathogenesis of SARS-CoV-2

Ashary

Bhide

Chakraborty

et al. 2020

Front. Cell Dev. Biol.

109

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show abstract

“…By contrast, the rodent labyrinthine placenta establishes an efficient counter-current maternal-fetal blood flow that minimizes hypoxia-reoxygenation stress to cells [190,191]. Human trophoblasts are also more invasive than rodent trophoblasts, and unlike rodent trophoblast giant cells, human EVT are thought to contribute more to uterine artery remodeling [190,192]. How or if such structural and physiological differences affect inflammatory processes (i.e., cytokine half-life, clearance, accessibility) is at this point not well understood.…”

Section: Impact Of Maternal Obesity On Placentationmentioning

confidence: 99%

Maternal Obesity and the Uterine Immune Cell Landscape: The Shaping Role of Inflammation

St-Germain

Castellana

Baltayeva

et al. 2020

IJMS

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Inflammation is often equated to the physiological response to injury or infection. Inflammatory responses defined by cytokine storms control cellular mechanisms that can either resolve quickly (i.e., acute inflammation) or remain prolonged and unabated (i.e., chronic inflammation). Perhaps less well-appreciated is the importance of inflammatory processes central to healthy pregnancy, including implantation, early stages of placentation, and parturition. Pregnancy juxtaposed with disease can lead to the perpetuation of aberrant inflammation that likely contributes to or potentiates maternal morbidity and poor fetal outcome. Maternal obesity, a prevalent condition within women of reproductive age, associates with increased risk of developing multiple pregnancy disorders. Importantly, chronic low-grade inflammation is thought to underlie the development of obesity-related obstetric and perinatal complications. While diverse subsets of uterine immune cells play central roles in initiating and maintaining healthy pregnancy, uterine leukocyte dysfunction as a result of maternal obesity may underpin the development of pregnancy disorders. In this review we discuss the current knowledge related to the impact of maternal obesity and obesity-associated inflammation on uterine immune cell function, utero-placental establishment, and pregnancy health.

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“…The reduction of arterial contractility caused by arterial reconstruction facilitates adequate maternal blood flow into the intervillous spaces [135]. Failure of this process will lead to an insufficient blood supply and cause placental dysfunction and preeclampsia in the late stage of pregnancy [136].…”

Section: Regulation Of Extravillous Trophoblast (Evt) Invasion By Embmentioning

confidence: 99%

Promoting Roles of Embryonic Signals in Embryo Implantation and Placentation in Cooperation with Endocrine and Immune Systems

Fujiwara

Ono

Sato

et al. 2020

IJMS

Self Cite

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Embryo implantation in the uterus is an essential process for successful pregnancy in mammals. In general, the endocrine system induces sufficient embryo receptivity in the endometrium, where adhesion-promoting molecules increase and adhesion-inhibitory molecules decrease. Although the precise mechanisms remain unknown, it is widely accepted that maternal–embryo communications, including embryonic signals, improve the receptive ability of the sex steroid hormone-primed endometrium. The embryo may utilize repulsive forces produced by an Eph–ephrin system for its timely attachment to and subsequent invasion through the endometrial epithelial layer. Importantly, the embryonic signals are considered to act on maternal immune cells to induce immune tolerance. They also elicit local inflammation that promotes endometrial differentiation and maternal tissue remodeling during embryo implantation and placentation. Additional clarification of the immune control mechanisms by embryonic signals, such as human chorionic gonadotropin, pre-implantation factor, zona pellucida degradation products, and laeverin, will aid in the further development of immunotherapy to minimize implantation failure in the future.

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Endovascular trophoblast and spiral artery remodeling

Cited by 82 publications

References 51 publications

Single-Cell RNA-seq Identifies Cell Subsets in Human Placenta That Highly Expresses Factors Driving Pathogenesis of SARS-CoV-2

Single-Cell RNA-seq Identifies Cell Subsets in Human Placenta That Highly Expresses Factors Driving Pathogenesis of SARS-CoV-2

Maternal Obesity and the Uterine Immune Cell Landscape: The Shaping Role of Inflammation

Promoting Roles of Embryonic Signals in Embryo Implantation and Placentation in Cooperation with Endocrine and Immune Systems

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