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Journal ArticleDOI

Cell Migration in BeWo Cells and the Role of Epithelial Sodium Channels

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TLDR
Immunocytochemistry studies showed that the three ENaC subunits showed greater expression at the leading edge of the wound 3 h after injury, supporting the notion that these proteins participate in a postinjury signal.
Abstract
Cell migration/proliferation processes associated with wound healing were measured in BeWo cells at 6 h, when mitosis is still scarce. Cells were cultured in medium with 1% fetal bovine serum to minimize proliferation. BeWo cell migration covered 20.6 ± 7.0%, 38.0 ± 5.4%, 16.6 ± 4.8% and 13.7 ± 3.6% of the wound when cultivated under control, aldosterone (100 nM, 12 h), aldosterone plus amiloride (10 μM) and amiloride treatments, respectively. When BeWo cells were treated with aldosterone, there was an increase in wound healing (P < 0.05), which was prevented by adding the ENaC blocker amiloride (P < 0.05, n = 16). Immunocytochemistry studies showed that the three ENaC subunits showed greater expression at the leading edge of the wound 3 h after injury, supporting the notion that these proteins participate in a postinjury signal. Antisense oligonucleotides directed against the α-ENaC subunit decreased the migratory response of the cells compared to the sense treated cells or the cells without oligonucleotides (P < 0.001, n = 16): 30.2 ± 3.7%, 17.6 ± 1.3%, 27.5 ± 1.5% and 20.2 ± 1.5% reinvasion of the wound with aldosterone, aldosterone plus antisense, aldosterone plus sense treatments and control conditions, respectively. Aldosterone and amiloride influence wound healing in BeWo cells, probably by their effects upon ENaCs, transmitting a signal to the cell cytoplasm for the release of several agents that promote cell migration.

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Journal ArticleDOI

Role of Ion Channels and Transporters in Cell Migration

TL;DR: After presenting general principles by which transport proteins affect cell migration, the role of channels and transporters involved in cell migration is discussed systematically.
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Sodium homeostasis in the tumour microenvironment.

TL;DR: Evidence indicating that Na+ handling is altered in tumours is reviewed, the current understanding of the mechanisms that may underlie these alterations are explored and the potential consequences for cancer progression are considered.
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Glioma-specific Cation Conductance Regulates Migration and Cell Cycle Progression

TL;DR: The data suggest that a specific cation conductance composed of acid-sensing ion channels and ENaC subunits regulates migration and cell cycle progression in gliomas.
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The epithelial sodium channel mediates the directionality of galvanotaxis in human keratinocytes

TL;DR: Evidence is provided that ENaC is required for directional migration of keratinocytes in an electric field, supporting a role for ENac in skin wound healing and suggesting that the channel open state is responsible for the response.
Journal ArticleDOI

ENaCs and ASICs as therapeutic targets

TL;DR: The known and potential roles of ENaC and ASIC subunits in the wide variety of pathologies in which these channels have been implicated are discussed.
References
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Pre-eclampsia

Journal ArticleDOI

Actin-Based Cell Motility and Cell Locomotion

TL;DR: This work acknowledges key intellectual contributions from Jody Rosenblatt and Julie Theriot (protrusion, Listeria motility) and attempted to fairly represent different laboratories, systems, and opinions.
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Epithelial sodium channel/degenerin family of ion channels: a variety of functions for a shared structure.

TL;DR: The functional heterogeneity among the members of the ENaC/DEG channel family provides a unique opportunity to address the molecular basis of basic channel functions such as activation by ligands, mechanotransduction, ionic selectivity, or block by pharmacological ligands.
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Placental Origins of Preeclampsia Challenging the Current Hypothesis

TL;DR: Although the placenta plays a crucial role in the development of preeclampsia, the onset, severity, and progression is significantly affected by the maternal response to placentally derived factors and proteins.
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Pre-eclampsia, the placenta and the maternal systemic inflammatory response--a review.

TL;DR: Evidence is presented that apoptotic or necrotic debris shed from the syncytial surface of the placenta constitutes the inflammatory stimulus in all pregnancies, which explains many features of pre-eclampsia including its occurrence with either larger placentae or small oxidatively stressed placente.
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