Morphologic and proteomic characterization of exosomes released by cultured extravillous trophoblast cells

Atay, Safinur; Gerçel-Taylor, Çiçek; Kesımer, Mehmet; Taylor, Douglas D.

doi:10.1016/j.yexcr.2011.01.014

Cited by 143 publications

(141 citation statements)

References 34 publications

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“…CD81 is a main component of exosomes in many cell types (10)(11)(12)24). Based on its association with the cellular membrane, CD81 can be found in either a soluble or insoluble form (12).…”

Section: Cd81 Expression Is Up-regulated In the Placentas And Maternamentioning

confidence: 99%

“…CD81 is also a tumor suppressor that inhibits the migration and invasion of some malignant tumor cells (8,9). In addition, an increasing number of studies have reported that CD81 is one of the main components of exosomes and can be released into maternal circulation or delivered to certain organs and tissues (10)(11)(12). Our previous study showed that CD81 is highly expressed in LPS-treated HTR-8/SV neo cells derived from human first TM extravillous trophoblast cells and induces trophoblast syncytialization (13); however, the role of CD81 in human placentation and PE development remains unknown.…”

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confidence: 99%

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Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

Shen

Diao

Sun

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Preeclampsia (PE) is initiated by abnormal placentation in the early stages of pregnancy, followed by systemic activation of endothelial cells of the maternal small arterioles in the late second or third trimester (TM) of pregnancy. During normal pregnancy, placental cytotrophoblasts (CTBs) invade the maternal uterine wall and spiral arteries, whereas this process is interrupted in PE. However, it is not known how the malformed placenta triggers maternal endothelial crisis and the associated manifestations. Here, we have focused on the association of CD81 with PE. CD81, a member of the tetraspanin superfamily, plays significant roles in cell growth, adhesion, and motility. The function of CD81 in human placentation and its association with pregnancy complications are currently unknown. In the present study, we have demonstrated that CD81 was preferentially expressed in normal first TM placentas and progressively downregulated with gestation advance. In patients with early-onset severe PE (sPE), CD81 expression was significantly up-regulated in syncytiotrophoblasts (STBs), CTBs and the cells in the villous core. In addition, high levels of CD81 were observed in the maternal sera of patients with sPE. Overexpressing CD81 in CTBs significantly decreased CTB invasion, and culturing primary human umbilical vein endothelial cells (HUVECs) in the presence of a high dose of exogenous CD81 resulted in interrupted angiogenesis and endothelial cell activation in vitro. Importantly, the phenotype of human PE was mimicked in the CD81-induced rat model.is characterized by a new onset of hypertension and proteinuria after 20 wk of gestation. Early-onset severe PE (sPE, ≤ 34 wk) is associated with a high incidence of eclampsia, cerebrovascular complications, and fetal growth restriction, which severely threaten maternal and fetal health (1). Although the etiology of PE remains elusive, this disease has two known stages: In stage I, inadequate cytotrophoblast (CTB) invasion early in the pregnancy causes abnormal placentation; in stage II, systemic endothelial cell activation and clinical manifestations occur in the second or third trimester (TM), which are associated with the release of molecules and factors from the shallowly implanted placenta (2, 3).CD81 is a widely expressed tetraspanin that provides a scaffold for signaling molecules and orchestrates interactions between membrane-associated proteins to initiate signaling cascades that regulate cell adhesion, migration, and invasion (4-7). CD81 is also a tumor suppressor that inhibits the migration and invasion of some malignant tumor cells (8, 9). In addition, an increasing number of studies have reported that CD81 is one of the main components of exosomes and can be released into maternal circulation or delivered to certain organs and tissues (10-12). Our previous study showed that CD81 is highly expressed in LPS-treated HTR-8/SV neo cells derived from human first TM extravillous trophoblast cells and induces trophoblast syncytialization (13); however, the role of CD81 in ...

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“…CD81 is a main component of exosomes in many cell types (10)(11)(12)24). Based on its association with the cellular membrane, CD81 can be found in either a soluble or insoluble form (12).…”

Section: Cd81 Expression Is Up-regulated In the Placentas And Maternamentioning

confidence: 99%

mentioning

confidence: 99%

Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

Shen

Diao

Sun

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…In has been suggested that the risk of preeclampsia could associate with an altered relation between various phenotypes of PCDE. The circulating exosomes regulating fetal vascular response play a pivotal role in mobbing progenitor precursors, endothelial dysfunction, cell proliferation, inflammation, vasculogenesis and neoangiogenesis [4,5]. They are key factors contributing in endogenous vascular reparative processes and adaptation to hypoxia / ischemia-induced injury of cytotrophoblast [5].…”

Section: Abstract: Pregnancy; Preeclampsia; Exosomes; Vascular Complimentioning

confidence: 99%

“…The circulating exosomes regulating fetal vascular response play a pivotal role in mobbing progenitor precursors, endothelial dysfunction, cell proliferation, inflammation, vasculogenesis and neoangiogenesis [4,5]. They are key factors contributing in endogenous vascular reparative processes and adaptation to hypoxia / ischemia-induced injury of cytotrophoblast [5]. Depending on their origin (activated or apoptotic fetal cells) exosomes appear to be distinguished in morphology, immune phenotypes, abilities to cargo some molecules (active proteins, pro-coagulants, growth factors, lipids, enzymes, micro-RNAs) and induce autocrine / paracrine effects on vasculature and trophoblast [6,7].…”

Section: Abstract: Pregnancy; Preeclampsia; Exosomes; Vascular Complimentioning

confidence: 99%

Are Placental Cell-Derived Exosomes a Predictive Biomarker of Preeclampsia?

Berezin¹

2017

Med chem

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Placenta is endocrine organ that regulate biological function of several maternal tissues and fetal organs by specific mechanisms of cell-to-cell cooperation, which is realized via exosomes' secretion. Exosomes delivery some molecules, i.e., active proteins, pro-coagulants, growth factors, lipids, enzymes, micro-RNAs to target cells and induce autocrine / paracrine effects on vasculature and trophoblast. Interestingly, circulating number of exosomes derived from placenta cells in healthy pregnancies increases in 50-100 fold times to healthy volunteers and they may be detected in several biological fluids across all gestation age starting with 6 weeks of gestation. Moreover, pregnancies at risk of preeclampsia exhibit extremely increased levels of total exosomes and placental cell-derived-exosomes in blood when compared with woman at risk free of preeclampsia. Taking into consideration this fact, measure of circulating number of placental cell-derived-exosomes could be an individual probe for personification of a risk of life-threatening event across pregnancy. The short communication is depicted the role of placental cell-derived-exosomes as biomarker of preeclampsia in asymptomatic pregnancies.

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“…This profile is generally produced by infiltrating macrophages following interactions with tumours or their components. While we proposed that exosomes could 'educate' macrophages to produce pro-inflammatory cytokines following internalization, we recently demonstrated that the induction of IL-1b was observed even when internalization of vesicles was blocked [59]. Arginine, glycine and aspartate containing peptides (RGD peptides), which are used to block fibronectin binding to macrophage a5b1 integrin, were observed to abrogate vesicle induction of IL-1b production and downstream phosphorylation of Akt and c-Jun [60].…”

Section: Functions Of Exosomesmentioning

confidence: 99%

Exosome platform for diagnosis and monitoring of traumatic brain injury

Taylor

Gerçel-Taylor

2014

Phil. Trans. R. Soc. B

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We have previously demonstrated the release of membranous structures by cells into their extracellular environment, which are termed exosomes, microvesicles or extracellular vesicles depending on specific characteristics, including size, composition and biogenesis pathway. With activation, injury, stress, transformation or infection, cells express proteins and RNAs associated with the cellular responses to these events. The exosomes released by these cells can exhibit an array of proteins, lipids and nucleic acids linked to these physiologic events. This review focuses on exosomes associated with traumatic brain injury, which may be both diagnostic and a causative factor in the progression of the injury. Based on current data, exosomes play essential roles as conveyers of intercellular communication and mediators of many of the pathological conditions associated with development, progression and therapeutic failures and cellular stress in a variety of pathologic conditions. These extracellular vesicles express components responsible for angiogenesis promotion, stromal remodelling, signal pathway activation through growth factor/receptor transfer, chemoresistance, immunologic activation and genetic exchange. These circulating exosomes not only represent a central mediator of the pro-inflammatory microenvironment linked with secondary brain injury, but their presence in the peripheral circulation may serve as a surrogate for biopsies, enabling real-time diagnosis and monitoring of neurodegenerative progression.

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Morphologic and proteomic characterization of exosomes released by cultured extravillous trophoblast cells

Cited by 143 publications

References 34 publications

Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

Are Placental Cell-Derived Exosomes a Predictive Biomarker of Preeclampsia?

Exosome platform for diagnosis and monitoring of traumatic brain injury

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