Protecting fetal development

Kellam, Paul; Weiss, Robin A.

doi:10.1126/science.aay2054

Cited by 5 publications

(1 citation statement)

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“…Cell fusion, also called syncytialization, is a specialized cellular event which occurs in multicellular organisms, both in physiological and pathological states (Chen & Olson 2005, Larsson et al 2008. During human placental development, the syncytiotrophoblast (STB) formed from the fusion of mononuclear cytotrophoblast (CTB) cells is responsible for the exchange of nutrients, gas, and waste products between the mother and the fetus (Ockleford & Whyte 1977, Kellam & Weiss 2019. It secretes hormones to maintain pregnancy and plays an important role in protecting the fetus from toxins and pathogens (Robbins et al 2010, Burton & Fowden 2015, Maltepe & Fisher 2015.…”

Section: Introductionmentioning

confidence: 99%

Appropriate expression of P57kip2 drives trophoblast fusion via cell cycle arrest

et al. 2021

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The syncytiotrophoblast, derived from cytotrophoblast fusion, is responsible for maternal–fetal exchanges, secretion of pregnancy-related hormones, and fetal defense against pathogens. Inadequate cytotrophoblast fusion can lead to pregnancy disorders, such as preeclampsia and fetal growth restriction. However, little is known about the mechanism of cytotrophoblast fusion in both physiological and pathological pregnancy conditions. In this study, P57kip2 (P57), a cell cycle-dependent kinase inhibitor that negatively regulates the cell cycle, was found to be up-regulated during the process of syncytialization in both primary trophoblast cells and BeWo cells. Co-immunofluorescence with proliferation markers Ki67 and Cyclin-CDK factors further showed that P57 specifically localizes in the post-mitotic cytotrophoblast subtype of the early pregnancy villi. Overexpression of P57 promoted trophoblast syncytialization by arresting the cell cycle at the G1/G0 phase and inhibiting proliferation. Blocking of the cell cycle through a serum starvation culture resulted in an enhancement of cytotrophoblast fusion and the up-regulation of P57. In both spontaneous cytotrophoblast fusion and forskolin-induced BeWo cell fusion models, an initial up-regulation of P57 was observed followed by a subsequent down-regulation. These findings indicate that proper expression of P57 at cytotrophoblast differentiation nodes plays an important role in trophoblast syncytialization.

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Section: Introductionmentioning

confidence: 99%

Appropriate expression of P57kip2 drives trophoblast fusion via cell cycle arrest

et al. 2021

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Immune Cycle‐Based Strategies for Cancer Immunotherapy

Liu

Zhang

et al. 2021

Adv Funct Materials

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The immune system is composed of immune organs, immune cells, and immunoactive substances, which plays a vital role in antitumor immunity in cancer immunotherapy. During the process of the antitumor immune response, many factors are involved in the cancer immune cycle. Therefore, developing intelligent strategies based on the steps of the cancer immune cycle to elicit the immune responses for enhanced cancer immunotherapy is of great significance. In this review, the key factors in each step of the cancer immune cycle are discussed, and then, the intelligent therapeutic strategies for modulating the immune surveillance against cancer are highlighted. Considering the demand for cancer immunotherapy in clinic, some suggestions for constructing new intelligent strategies are also put forward, which will make antitumor immunity more effective and advance the development of cancer immunotherapy.

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Comparative analysis reveals adaptive evolution of bat IFITMs and a novel antiviral determinant

Benfield

MacKenzie

Ritzefeld

et al. 2019

Preprint

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doi: bioRxiv preprint 65 required for the antiviral activity of both IFITM3 and IFITM1 [9]. The subcellular localization of 66 IFITMs is a key determinant of their antiviral profile. When expressed singly, IFITM3 and IFITM2 67 preferentially localize to early and late endosomes and lysosomes, and restrict viruses that enter via 68 these endo-lysosomal compartments. In contrast, IFITM1 primarily localizes at the cell surface and 69 can restrict viruses that enter through the plasma membrane [11-14]. Indeed, mutants of IFITM3 70 that lack an N-terminal endocytic sorting motif 20 YEML 23 localize to the plasma membrane and lose 71 their ability to inhibit influenza A virus (IAV), alphavirus and coronavirus infection by endosomal 72 routes [14-18]. 73 74 Studies focusing on IFITM3 restriction of IAV and Semliki Forest Virus (SFV) indicate that virus 75 internalization is unaffected by IFITM3 expression and, for SFV at least, the viral envelope 76 . CC-BY-NC-ND 4.0 International license author/funder. It is made available under a The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/737841 doi: bioRxiv preprint 109 knockout mice show enhanced morbidity after infection with IAV, alphaviruses and flaviviruses [33-110 .

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Protecting fetal development

Abstract: Control of cell fusion in the placenta affects the balance between health and harm

Cited by 5 publications

References 14 publications

Appropriate expression of P57kip2 drives trophoblast fusion via cell cycle arrest

Appropriate expression of P57kip2 drives trophoblast fusion via cell cycle arrest

Immune Cycle‐Based Strategies for Cancer Immunotherapy

Comparative analysis reveals adaptive evolution of bat IFITMs and a novel antiviral determinant

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