Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A fully iPS-cell-derived 3D model of the human blood-brain barrier for exploring neurovascular disease mechanisms and therapeutic interventions.

Nature neuroscience·2025
Same author

The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling.

Nature neuroscience·2025
Same author

Plasmodium falciparum impairs Ang-1 secretion by pericytes in a 3D brain microvessel model.

EMBO molecular medicine·2025
Same author

Stage-dependent expression and vacuolar localization of Plasmodium berghei chloroquine resistance transporter (CRT).

Molecular and biochemical parasitology·2025
Same author

Febrile temperature enhances <i>Plasmodium falciparum</i> cytoadhesion by disrupting the endothelial glycocalyx.

bioRxiv : the preprint server for biology·2025
Same author

Plasmodium falciparum egress disrupts endothelial junctions and activates JAK-STAT signaling in a microvascular 3D blood-brain barrier model.

Nature communications·2025
Same journal

OTUB1 non-canonically inhibits TAB2 ubiquitination to govern microglia-mediated neuroinflammation.

EMBO molecular medicine·2026
Same journal

Impaired gephyrin G-domain trimerization and phase separation in a patient with developmental epileptic encephalopathy.

EMBO molecular medicine·2026
Same journal

Single-nuclei UPR profiling by flow cytometry reveals bortezomib resistance mechanisms in multiple myeloma.

EMBO molecular medicine·2026
Same journal

Anle138b ameliorates pathological phenotypes in mouse and cellular models of Huntington's disease.

EMBO molecular medicine·2026
Same journal

Bacterialized tumor cells as vaccine.

EMBO molecular medicine·2026
Same journal

Activation of AMPK as a therapeutic strategy for FBXL4-related mitochondrial DNA depletion syndrome.

EMBO molecular medicine·2026
See all related articles

Related Experiment Video

Updated: Jun 16, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
09:04

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging

Published on: June 8, 2017

ETS-guided iPSC-endothelial models recapitulate malaria pathogenesis.

François Korbmacher1, Rory K M Long1,2, Hannah Fleckenstein1,3

  • 1European Molecular Biology Laboratory (EMBL) Barcelona, Barcelona, Spain.

EMBO Molecular Medicine
|June 13, 2026
PubMed
Summary
This summary is machine-generated.

Severe malaria involves parasite sequestration in blood vessels. Researchers developed a new stem cell model (ETS-iBMEC) to better study how malaria parasites infect human cells and disrupt blood vessel function.

More Related Videos

An Experimental Model to Study Tuberculosis-Malaria Coinfection upon Natural Transmission of Mycobacterium tuberculosis and Plasmodium berghei
09:02

An Experimental Model to Study Tuberculosis-Malaria Coinfection upon Natural Transmission of Mycobacterium tuberculosis and Plasmodium berghei

Published on: February 17, 2014

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
10:09

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells

Published on: January 3, 2012

Related Experiment Videos

Last Updated: Jun 16, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
09:04

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging

Published on: June 8, 2017

An Experimental Model to Study Tuberculosis-Malaria Coinfection upon Natural Transmission of Mycobacterium tuberculosis and Plasmodium berghei
09:02

An Experimental Model to Study Tuberculosis-Malaria Coinfection upon Natural Transmission of Mycobacterium tuberculosis and Plasmodium berghei

Published on: February 17, 2014

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
10:09

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells

Published on: January 3, 2012

Area of Science:

  • Vascular Biology
  • Infectious Diseases
  • Stem Cell Biology

Background:

  • Severe malaria pathogenesis is poorly understood due to Plasmodium falciparum's human specificity.
  • Microvasculature sequestration of malaria parasites drives severe disease.
  • Induced pluripotent stem cell (iPSC) technology offers a model for studying parasite-host interactions.

Purpose of the Study:

  • To develop an improved in vitro model for studying malaria parasite-host interactions in the human vasculature.
  • To generate an iPSC-derived endothelial cell line with enhanced endothelial identity and barrier function.

Main Methods:

  • Generated a novel iPSC line (ETS-iBMEC) with inducible expression of ETS transcription factors (ETV2, FLI1, ERG).
  • Assessed endothelial identity, barrier function, and binding of infected cells to ETS-iBMEC.
  • Analyzed transcriptional changes in response to parasite products, focusing on metabolic, splicing, and vascular pathways.

Main Results:

  • ETS-iBMEC exhibited improved endothelial identity and strong barrier function.
  • High binding of Plasmodium falciparum-infected red blood cells and neutrophils to ETS-iBMEC was observed.
  • Parasite products induced significant transcriptional changes in metabolic, splicing, and endothelial barrier/angiogenic pathways.
  • Confirmed the angiopoietin-Tie2 axis role and identified new pathways like VEGF-Notch signalling in parasite-mediated barrier disruption.

Conclusions:

  • The novel ETS-iBMEC iPSC-based model provides a robust platform for studying human vascular infections, particularly malaria.
  • This model advances understanding of parasite sequestration and its impact on endothelial barrier function.
  • The study highlights key molecular pathways involved in malaria-induced vascular dysfunction, offering potential therapeutic targets.