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The Blood-brain Barrier

The Blood-brain Barrier

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Related Experiment Video

Updated: Sep 20, 2025

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

RGMa Participates in the Blood-Brain Barrier Dysfunction Through BMP/BMPR/YAP Signaling in Multiple Sclerosis.

Lei Zhang¹, Shi Tang¹, Yue Ma¹

¹Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Frontiers in Immunology

|June 6, 2022

Summary

Repulsive guidance molecule-a (RGMa) disrupts the blood-brain barrier (BBB) in multiple sclerosis (MS) by activating the BMP2/BMPR II/YAP pathway, offering a new therapeutic target for MS.

Keywords:

blood–brain barrier bone morphogenetic protein multiple sclerosis repulsive guidance molecule-a yes-associated protein

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Last Updated: Sep 20, 2025

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Area of Science:

Neuroimmunology
Vascular Biology
Cellular Signaling

Background:

The blood-brain barrier (BBB) dysfunction is critical in multiple sclerosis (MS) pathogenesis, but underlying mechanisms remain unclear.
Repulsive guidance molecule-a (RGMa) is implicated in MS, yet its precise role in BBB integrity requires further investigation.

Purpose of the Study:

To investigate RGMa's role in regulating BBB permeability in endothelial cells and MS.
To elucidate the molecular mechanisms by which RGMa influences BBB integrity.

Main Methods:

Established an experimental autoimmune encephalomyelitis (EAE) mouse model and human brain microvascular endothelial cell (HBMEC) cultures.
Assessed BBB permeability via RGMa overexpression and knockdown, and analyzed signaling pathways involving BMP2/BMPRII and YAP.
Measured RGMa levels in MS patients with and without contrast-enhancing lesions.

Main Results:

RGMa, BMP2/BMPRII, and YAP expression correlated with BBB disruption in EAE mice and HBMECs.
RGMa overexpression increased BBB permeability, while RGMa knockdown enhanced BBB integrity in vitro.
RGMa-induced BBB dysfunction involves the BMP2/BMPRII/YAP pathway, leading to decreased tight junction proteins (ZO-1, claudin-5).
Elevated serum RGMa levels were observed in MS patients, particularly those with active lesions.

Conclusions:

RGMa drives BBB dysfunction in MS via the BMP2/BMPRII/YAP signaling cascade.
RGMa represents a potential therapeutic target for managing BBB permeability in multiple sclerosis.