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

Cell Migration01:19

Cell Migration

6.7K
Cell migration is a process by which the cells move from one location to another, playing an essential role in embryological development, repair and regeneration, immune response, and metastasis. Cells migrate in response to chemical or mechanical signals generated by specific organs or tissues. The overall mechanism includes three steps - polarization, protrusion, and release. Polarization involves the formation of a distinct cell front and rear, which determines the direction of movement.
6.7K
Cell Migration01:09

Cell Migration

18.9K
Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.
18.9K
Binet's Contribution to Measures of Intelligence01:23

Binet's Contribution to Measures of Intelligence

1.8K
Alfred Binet, along with his student Théophile Simon, was tasked by the French Ministry of Education in 1904 to create a method for identifying students who struggled to learn through conventional classroom instruction. This initiative aimed to address overcrowding by placing such students in specialized schools. Binet and Simon developed an intelligence test comprising 30 tasks, ranging from simple commands, like touching one's nose or ear, to more complex tasks, such as drawing...
1.8K
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

3.3K
Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
3.3K
Chemotaxis and Direction of Cell Migration01:21

Chemotaxis and Direction of Cell Migration

5.8K
Cells can detect chemical cues in their environment and reorganize the cytoskeleton to migrate toward them or away from them. This directional migration, called chemotaxis, is essential during embryogenesis and development, immune response, tissue repair and regeneration, and reproduction. These chemical cues can either attract or repel the cell's movement. For example, axon development is determined by a combination of chemoattractants and chemorepellents that direct the growing axon...
5.8K
Role of Myosin in Cell Migration01:18

Role of Myosin in Cell Migration

3.4K
Myosins are multimeric motor proteins involved in various cellular processes such as migration, adhesion, and proliferation. Myosin II is the most common type in animal cells, which binds and cross-links actin filaments.
Myosin II  is a hexamer comprising two heavy chains with globular heads and coiled-coil tails, two regulatory light chains, and two essential light chains. The ATPase sites on the myosin heads hydrolyze ATP, and the released phosphate generates the force for contraction....
3.4K

You might also read

Related Articles

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

Sort by
Same author

Cyclophilin A (CyPA) induces chemotaxis independent of its peptidylprolyl cis-trans isomerase activity: direct binding between CyPA and the ectodomain of CD147.

The Journal of biological chemistry·2011
Same author

Characterization of dissolved organic matter in urban sewage using excitation emission matrix fluorescence spectroscopy and parallel factor analysis.

Journal of environmental sciences (China)·2011
Same author

Actin filament associated protein mediates c-Src related SRE/AP-1 transcriptional activation.

FEBS letters·2011
Same author

Sesquiterpenes from Vladimiria souliei and their inhibitory effects on NO production.

Fitoterapia·2011
Same author

Chronic kidney disease is prevalent in Chinese patients admitted with verified cerebrovascular lesions and predicts short-term prognosis.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2011
Same author

Cytoprotective effects of albumin, nitrosated or reduced, in cultured rat pulmonary vascular cells.

American journal of physiology. Lung cellular and molecular physiology·2011

Related Experiment Video

Updated: Feb 15, 2026

Assessment of Endothelial Cell Migration After Exposure to Toxic Chemicals
07:07

Assessment of Endothelial Cell Migration After Exposure to Toxic Chemicals

Published on: July 10, 2015

9.2K

The interaction between XBP1 and eNOS contributes to endothelial cell migration.

Junyao Yang1, Jing Xu2, Martin Danniel3

  • 1Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China; Cardiovascular Division, Faculty of Life Science and Medicine, King's College London, SE5 9NU London, United Kingdom.

Experimental Cell Research
|January 22, 2018
PubMed
Summary

X-box binding protein 1 (XBP1) splicing regulates endothelial cell migration by up-regulating nitric oxide synthase 3 (eNOS). This process is crucial for wound healing and angiogenesis, involving the Akt signaling pathway and miR-24.

Keywords:
Cell migrationEndothelial cellMicroRNANitric oxide synthaseX-box binding protein 1

More Related Videos

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

3.9K
Migration, Chemo-Attraction, and Co-Culture Assays for Human Stem Cell-Derived Endothelial Cells and GABAergic Neurons
10:09

Migration, Chemo-Attraction, and Co-Culture Assays for Human Stem Cell-Derived Endothelial Cells and GABAergic Neurons

Published on: January 23, 2020

7.5K

Related Experiment Videos

Last Updated: Feb 15, 2026

Assessment of Endothelial Cell Migration After Exposure to Toxic Chemicals
07:07

Assessment of Endothelial Cell Migration After Exposure to Toxic Chemicals

Published on: July 10, 2015

9.2K
A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

3.9K
Migration, Chemo-Attraction, and Co-Culture Assays for Human Stem Cell-Derived Endothelial Cells and GABAergic Neurons
10:09

Migration, Chemo-Attraction, and Co-Culture Assays for Human Stem Cell-Derived Endothelial Cells and GABAergic Neurons

Published on: January 23, 2020

7.5K

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • X-box binding protein 1 (XBP1) is a key regulator of the endoplasmic reticulum stress response.
  • Previous research links XBP1 to vascular endothelial growth factor (VEGF)-mediated endothelial cell (EC) proliferation and angiogenesis.

Purpose of the Study:

  • To investigate the role of XBP1 splicing in endothelial cell migration.
  • To elucidate the molecular mechanisms underlying XBP1-mediated EC migration.

Main Methods:

  • EC monolayer wound healing, tube formation, and transwell migration assays.
  • Gene manipulation using Ad-XBP1s and ShRNA lentivirus for XBP1 and IRE1α.
  • mRNA stabilization assays, co-immunoprecipitation, and immunofluorescence staining.

Main Results:

  • EC scratching induced XBP1 splicing, modulated by VEGF signaling inhibitors.
  • Overexpression of spliced XBP1 (XBP1s) enhanced EC migration, while knockdown suppressed it.
  • XBP1s upregulated nitric oxide synthase 3 (NOS3/eNOS) via 3'UTR stabilization and increased protein translation, involving miR-24.
  • XBP1s, Akt, and eNOS formed a complex, leading to nuclear translocation of Akt and eNOS.

Conclusions:

  • XBP1 splicing is a critical regulator of EC migration.
  • XBP1s influences eNOS expression and cellular localization, promoting EC migration.
  • The findings highlight a novel pathway involving XBP1s, Akt, eNOS, and miR-24 in EC migration, relevant to wound healing and angiogenesis.