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

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

4.7K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
4.7K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

4.4K
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.4K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

7.3K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.3K

You might also read

Related Articles

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

Sort by
Same author

Red ginseng-mediated modulation of the NLRP3 Inflammasome in neuroinflammatory-related cognitive impairments.

Journal of ginseng research·2026
Same author

De Novo Lipogenesis in Clear Cell Renal Cell Carcinoma: Mechanistic Insights and Therapeutic Implications.

International journal of molecular sciences·2026
Same author

An Experimental Study on the Effectiveness and Usefulness of 360° Virtual Reality Simulation in Korean Medical Education: A Pilot Study.

Healthcare (Basel, Switzerland)·2026
Same author

Roles of Lcn2 and neuroinflammation in a scopolamine-induced cognitive impairment animal model: implication of the NLRP3 inflammasome pathway.

Genes & genomics·2026
Same author

Gami-Guibitang Attenuates Anxiety-like Behaviors and Modulates Hippocampal Synaptic Signaling in a Valproic Acid-Induced Mouse Model of Autism.

Brain sciences·2026
Same author

Risk Factors for Postoperative Delirium in Nonintensive Care Unit Patients: Machine Learning Approach.

Computers, informatics, nursing : CIN·2026

Related Experiment Video

Updated: May 5, 2026

A Visual Description of the Dissection of the Cerebral Surface Vasculature and Associated Meninges and the Choroid Plexus from Rat Brain
12:31

A Visual Description of the Dissection of the Cerebral Surface Vasculature and Associated Meninges and the Choroid Plexus from Rat Brain

Published on: November 14, 2012

49.1K

Involvement of RhoA/ROCK Signaling Pathway in Methamphetamine-Induced Blood-Brain Barrier Disruption.

Jong Su Hwang1, Tam Thuy Lu Vo1, Mikyung Kim1

  • 1Department of Biochemistry, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.

Biomolecules
|March 28, 2025
PubMed
Summary

Methamphetamine (METH) disrupts the blood-brain barrier (BBB) by activating the RhoA/ROCK pathway. This pathway affects junction proteins and cytoskeletal organization, leading to BBB dysfunction in methamphetamine abuse.

Keywords:
RhoA/ROCK signaling pathwayY-27632blood–brain barriermethamphetamineprimary human brain microvascular endothelial cells

More Related Videos

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

17.6K
A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
07:56

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

Published on: August 11, 2021

2.6K

Related Experiment Videos

Last Updated: May 5, 2026

A Visual Description of the Dissection of the Cerebral Surface Vasculature and Associated Meninges and the Choroid Plexus from Rat Brain
12:31

A Visual Description of the Dissection of the Cerebral Surface Vasculature and Associated Meninges and the Choroid Plexus from Rat Brain

Published on: November 14, 2012

49.1K
A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

17.6K
A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
07:56

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

Published on: August 11, 2021

2.6K

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Methamphetamine (METH) abuse is a global health issue with significant neurotoxic effects.
  • Blood-brain barrier (BBB) dysfunction is increasingly recognized as a key factor in METH-induced brain pathology.
  • The precise mechanisms underlying METH-induced BBB disruption remain incompletely understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which METH impairs BBB integrity.
  • To investigate the role of the RhoA/ROCK signaling pathway in METH-induced BBB dysfunction.
  • To evaluate the therapeutic potential of ROCK inhibitors in mitigating METH-induced BBB damage.

Main Methods:

  • In vitro studies using primary human brain endothelial cells (HBMECs) exposed to METH.
  • Assessment of paracellular permeability using FITC-dextran and trans-endothelial electrical resistance (TEER) assays.
  • Analysis of tight junction protein expression (zonula occluden-1, claudin-5) and F-actin cytoskeleton.
  • Examination of RhoA/ROCK pathway activation, including phosphorylation of myosin light chain (MLC) and cofilin.
  • In vitro and in vivo evaluation of ROCK inhibitors (Y-27632, fasudil).

Main Results:

  • METH exposure increased paracellular permeability and decreased vascular integrity in HBMECs.
  • METH caused redistribution of tight junction proteins and F-actin cytoskeletal reorganization.
  • METH activated the RhoA/ROCK pathway, leading to increased phosphorylation of MLC and cofilin.
  • ROCK inhibitors prevented METH-induced changes in junction proteins and cytoskeleton, and alleviated BBB leakage in vitro and in vivo.

Conclusions:

  • METH induces blood-brain barrier dysfunction by activating the RhoA/ROCK signaling pathway.
  • Activation of RhoA/ROCK leads to F-actin cytoskeletal reorganization and altered tight junction protein distribution.
  • Targeting the RhoA/ROCK pathway with inhibitors shows promise for treating METH-induced BBB damage.