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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Isolation of Human Umbilical Vein Endothelial Cells (HUVEC)
09:19

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Published on: April 28, 2007

Enterococcus faecalis internalization in human umbilical vein endothelial cells (HUVEC).

Diana Millán1, Carlos Chiriboga, Manuel A Patarroyo

  • 1Tissue Engineering Group, Universidad Nacional de Colombia, Carrera 45#26-85, Bogotá, Colombia.

Microbial Pathogenesis
|November 24, 2012
PubMed
Summary

Enterococcus faecalis internalization into human umbilical vein endothelial cells involves cytoskeletal components but not the Asc10 protein. This study reveals partial involvement of cytoskeleton proteins in bacterial entry and increased cell apoptosis.

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Published on: August 8, 2012

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Enterococcus faecalis interactions with endothelial cells are crucial for infection but poorly understood.
  • The E. faecalis aggregation substance (AS) protein, Asc10, is implicated in virulence and bacterial persistence.
  • Endothelial cell models are needed to study E. faecalis adherence, colonization, and invasion.

Purpose of the Study:

  • To investigate the role of Asc10 and cytoskeletal proteins (microtubules, actin) in E. faecalis internalization by HUVECs.
  • To assess the impact of E. faecalis internalization on HUVEC apoptosis.

Main Methods:

  • Utilized in vitro models with cultured human umbilical vein endothelial cells (HUVECs).
  • Assessed the involvement of Asc10 and cytoskeletal components in E. faecalis entry into HUVECs.
  • Quantified HUVEC apoptosis following bacterial internalization.

Main Results:

  • Cytoskeleton components, including microtubules and actin microfilaments, were partially involved in E. faecalis entry into HUVECs.
  • E. faecalis internalization led to increased HUVEC apoptosis.
  • The Asc10 protein did not appear to be a critical factor for E. faecalis entry into cultured HUVECs.

Conclusions:

  • E. faecalis entry into endothelial cells is partially mediated by host cell cytoskeletal elements.
  • Asc10 is likely not a primary driver for E. faecalis endothelial cell invasion.
  • Bacterial entry into endothelial cells induces significant host cell apoptosis.