Embolism to the Lungs by Trophoblast

Attwood, H. D.; Park, W. W.

doi:10.1097/00006254-196204000-00002

Cited by 30 publications

(45 citation statements)

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“…There is growing evidence that placental vesicles may be involved in the pathogenesis of preeclampsia by carrying at least a component of the toxin(s) released from the placenta. It is well documented that there is an increase in shedding of placental macrovesicles (SNAs) during preeclampsia (Attwood and Park 1961;Chua et al 1991;Buurma et al 2013). Similarly, the shedding of placental microvesicles into the maternal blood is also increased in women with early onset preeclampsia (Goswami et al 2006;Chen et al 2012b), with levels in the maternal blood correlating with systolic blood pressure (Lok et al 2008b).…”

Section: The Production Of Placental Vesicles Is Increased In Preeclamentioning

confidence: 99%

Placental Extracellular Vesicles and Feto-Maternal Communication

Tong

Chamley

2015

Cold Spring Harbor Perspectives in Medicine

121

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The human placenta is an anatomically unique structure that extrudes a variety of extracellular vesicles into the maternal blood (including syncytial nuclear aggregates, microvesicles, and nanovesicles). Large quantities of extracellular vesicles are produced by the placenta in both healthy and diseased pregnancies. Since their first description more than 120 years ago, placental extracellular vesicles are only now being recognized as important carriers for proteins, lipids, and nucleic acids, which may play a crucial role in feto-maternal communication. Here, we summarize the current literature on the cargos of placental extracellular vesicles and the known effects of such vesicles on maternal cells/systems, especially those of the maternal immune and vascular systems.T he placenta is an unusual organ with a short and defined life span. The human placenta is a fetal organ that sits between the fetus and its mother, connecting the fetus to the maternal blood supply. It is highly invasive and the entire surface of the placenta is in contact with the maternal circulation during most of gestation. Therefore, the human placenta effectively behaves as one wall of a maternal "blood vessel." This phenomenon is quite remarkable because, being a fetal organ, the placenta is in essence a semiallogeneic tissue graft in normal pregnancy and a complete allograft in surrogate or donor egg pregnancies. Therefore, the placenta is nature's only tissue graft.The human placenta has a villous (branching) structure. The surface of placental villi is covered by the multinucleated syncytiotrophoblast that is terminally differentiated and is not mitotically active. The growth and replenishment of the syncytiotrophoblast is effected by fusion of underlying mononuclear cytotrophoblasts into this layer. Beneath the cytotrophoblasts is the mesenchymal core of the villus with fetal blood vessels. The syncytiotrophoblast is a remarkable cell, which at least in theory, is a single cell covering the entire surface of the placenta and is the immunological barrier between the maternal immune system and the fetus. In a normal term placenta, the syncytiotrophoblast has an area of some 11 -13 m 2 (Mayhew 2014). However, the syncytiotrophoblast can be denuded, leaving areas lined by fibrinoid rather than syncytiotrophoblast and presumably before the laying down of this fibrinoid, cells of the villous mesenchymal core or cytotrophoblasts are exposed to the maternal blood, at least temporarily.

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Section: The Production Of Placental Vesicles Is Increased In Preeclamentioning

confidence: 99%

Placental Extracellular Vesicles and Feto-Maternal Communication

Tong

Chamley

2015

Cold Spring Harbor Perspectives in Medicine

121

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“…Further work in vitro [44,45], provided evidence suggesting that the signaling between different populations can be mediated by soluble mediators which inhibit the survival of disseminated cells in some locations but not in others. Autopsy studies on humans [46,47] and animals [35] indicate that normal cells do not survive for more than a few days in ectopic locations, when disseminated by accident or by experimental design via the circulation and it seems likely that the local inhibitory mediators act as homeostatic regulators preventing formation of colonies in inappropriate locations. It follows that metastatic tumor cells have clearly found ways to circumvent these controls.…”

Section: Metastasismentioning

confidence: 99%

Clinical and Biological Implications of the Tumor Microenvironment

Tarin¹

2012

Cancer Microenvironment

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In normal tissues and organs, the activities of the constituent cells are strictly restricted to the tasks assigned to them during development. In addition they (with the exception of leukocytes) remain inflexibly confined to their territorial domains by regulatory interactions with their neighbors. This creates specialized local micro-environments in which structure and function are orderly, stable and tightly controlled by feed-back loops, within interacting regulatory networks. This system has considerable ability to adapt to changing conditions. In contrast, the microenvironment in regions where tumors are forming and expanding is characterized by progressive loss of specialized or differentiated cellular functions, disorderly molecular signals, degeneration of microscopical organ structure. This, coupled with the traffic of cells into and out of the tumor, often culminating in local invasion and metastasis to other organs. The nature of these disturbed molecular and cellular interactions is, by definition, highly unstable and increasingly unpredictable as time passes. It also varies between different tumors, sometimes even leading to regression. However, systematic analysis of this dysfunction in the tumor microcosm, using multiple modern research techniques, has revealed that all actively growing primary and secondary neoplasms share an absolute dependency upon support from adjacent non-neoplastic cells of the host. This support, in turn, continuously depends upon dynamic interplay between tumor and host cell populations, via signaling molecules and surface receptors in the tumor microenvironment. Such interplay determines the fate of the growing neoplasm. Such information, described and evaluated in this article, provides important new insights into the etiology of carcinogenesis and how tumor growth, invasion and metastasis might be therapeutically arrested. The facts and concepts assembled below, regarding the cancer microenvironment, demonstrate how modern molecular findings reveal the impact of the wide range of cancer diseases upon the internal cellular, tissue and organ environments of the whole individual and how this applies to designing new work to improve human cancer diagnosis and treatment. The article discusses several specific types of experimentally-induced and clinically common cancers to derive principles useful for interpreting events in the tumor microenvironment, which apply to cancers in general and especially to human malignant disease.

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“…Occasionally these groups were so large that they were visible as nodules protruding from the surface of the lung. The Trophoblastic Index (a measure of the abundance of these cells, see Attwood & Park, 1961) appeared to increase with the number of lung sections examined. Lung samples from five animals killed up to 2 months in the postpartum period also showed trophoblast embolism.…”

mentioning

confidence: 98%

“…Trophoblastic`sprouts' break away from the syncytium into the intervillous space and pass directly into the maternal venous system (Hamilton & Boyd, 1966). These cells can be found in the venous drainage of the uterus throughout most of pregnancy (Douglas, Thomas, Carr, Cullen & Morris, 1959) and, although many are subsequently destroyed, probably by some lytic action of the blood, considerable numbers reach the maternal lungs (Attwood & Park, 1961 (Hamilton & Boyd, 1966).…”

mentioning

confidence: 99%