Symbolic illustration of blood vessels and nerve fibers representing multiple sclerosis treatment.

Cracking the MS Code: How Targeting Blood Vessels Could Halt the Disease

Jordan Keane in Health & Wellness June 2025 • 4 min read.

"New Research Reveals the Critical Role of Blood Vessel Inflammation in Multiple Sclerosis Progression"

Multiple sclerosis (MS) is a devastating disease of the central nervous system, characterized by the body's immune system mistakenly attacking the protective myelin sheath around nerve fibers. This leads to a cascade of inflammation and damage, resulting in a wide range of neurological symptoms. While there's no cure for MS yet, ongoing research is tirelessly exploring ways to manage the disease, slow its progression, and ultimately, improve the lives of those affected.

Inflammation is a key villain in the MS story. It fuels the demyelination process and directly injures tissue. One of the inflammatory compounds implicated is prostaglandin E2 (PGE2). PGE2 is produced when the body is injured and controls inflammation by acting on certain cells. Recent studies are suggesting blood vessels play a critical role in this process in MS.

Now, exciting new research is shedding light on the intricate connection between blood vessel health and MS. Scientists have zeroed in on how a specific enzyme, microsomal prostaglandin E synthase-1 (mPGES-1), within blood vessels, influences the development of MS. By understanding this relationship, researchers hope to develop targeted therapies that can slow down the disease.

The Blood Vessel Connection: mPGES-1 and MS

Symbolic illustration of blood vessels and nerve fibers representing multiple sclerosis treatment.

The new research, published in the International Journal of Molecular Sciences, investigates how mPGES-1 affects blood vessels and the surrounding tissues in an animal model of MS called experimental autoimmune encephalomyelitis (EAE). Researchers compared mice with normal mPGES-1 levels to mice genetically engineered to lack mPGES-1. The findings revealed striking differences in how the disease progressed in the two groups.

The study revealed that mice with normal mPGES-1 showed increased blood vessel growth and inflammation in the spinal cord during EAE. This suggests that mPGES-1 promotes vascularity. Vascularity simply means the number and density of blood vessels in a given area. It can lead to more immune cells entering the central nervous system, fueling inflammation and worsening the disease. Further, the researchers discovered that endothelial interleukin-1ß (IL-1ß) production was also elevated in regular mice compared to mice lacking the enzyme. IL-1ß is another key inflammatory protein, suggesting mPGES-1 also boosts IL-1ß production.

The study highlights the following major points:

mPGES-1 promotes blood vessel growth (vascularity) in areas affected by MS.
mPGES-1 increases the production of the inflammatory protein IL-1ß in blood vessels.
The effects of mPGES-1 are mediated through specific receptors (EP receptors) on blood vessel cells.
Blocking mPGES-1 reduces vascularity and inflammation in the animal model of MS.

The researchers also explored how mPGES-1 exerts its effects on blood vessels. They found that mPGES-1 influences the expression of specific receptors, called E-prostanoid (EP) receptors, on the surface of blood vessel cells. IL-1ß was increased in EP receptor-positive cells. These receptors act like antennae, receiving signals from PGE2, and the researchers found that IL-1ß production was ramped up in blood vessel cells with these receptors. This suggests that mPGES-1-generated PGE2 is driving inflammation through these EP receptors. Moreover, IL-1 receptor 1 expression on vascular endothelial cells increased upon EAE induction. The findings indicate that mPGES-1 worsens EAE by increasing vascularity and boosting IL-1ß production in blood vessels.

Hope for New Treatments

This research offers a promising new avenue for MS treatment. By targeting mPGES-1, or the specific EP receptors it influences, researchers hope to develop therapies that can reduce blood vessel inflammation and slow down MS progression. These findings pave the way for innovative strategies to combat this debilitating disease.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.3390/ijms19113647, Alternate LINK

Title: Endothelial Microsomal Prostaglandin E Synthetase-1 Upregulates Vascularity And Endothelial Interleukin-1Β In Deteriorative Progression Of Experimental Autoimmune Encephalomyelitis

Subject: Inorganic Chemistry

Journal: International Journal of Molecular Sciences

Publisher: MDPI AG

Authors: Takako Takemiya, Marumi Kawakami, Chisen Takeuchi

Published: 2018-11-19

Everything You Need To Know

How are blood vessels connected to Multiple Sclerosis (MS) progression?

In Multiple Sclerosis (MS), the body's immune system mistakenly attacks the myelin sheath, leading to inflammation and damage. Recent research suggests that blood vessels play a critical role in this process. An enzyme within blood vessels, called microsomal prostaglandin E synthase-1 (mPGES-1), influences the development of MS. Researchers hope that by understanding this relationship, targeted therapies can be developed to slow down the disease.

What role does microsomal prostaglandin E synthase-1 (mPGES-1) play in the context of Multiple Sclerosis and blood vessel inflammation?

Microsomal prostaglandin E synthase-1 (mPGES-1) promotes blood vessel growth, also known as vascularity, in areas affected by MS. This increased vascularity allows more immune cells to enter the central nervous system, fueling inflammation and worsening the disease. Additionally, mPGES-1 increases the production of the inflammatory protein endothelial interleukin-1ß (IL-1ß) in blood vessels, further contributing to the inflammatory process.

How do E-prostanoid (EP) receptors contribute to the inflammatory process driven by microsomal prostaglandin E synthase-1 (mPGES-1) in Multiple Sclerosis?

The effects of microsomal prostaglandin E synthase-1 (mPGES-1) on blood vessels are mediated through specific receptors called E-prostanoid (EP) receptors on the surface of blood vessel cells. These EP receptors act like antennae, receiving signals from prostaglandin E2 (PGE2). The research found that endothelial interleukin-1ß (IL-1ß) production was ramped up in blood vessel cells with these EP receptors, suggesting that mPGES-1-generated prostaglandin E2 (PGE2) is driving inflammation through these receptors.

What are the potential therapeutic implications of targeting microsomal prostaglandin E synthase-1 (mPGES-1) or E-prostanoid (EP) receptors for Multiple Sclerosis treatment?

This research offers a potential avenue for Multiple Sclerosis (MS) treatment by targeting microsomal prostaglandin E synthase-1 (mPGES-1) or the specific E-prostanoid (EP) receptors it influences. Researchers hope to develop therapies that can reduce blood vessel inflammation and slow down MS progression. These findings pave the way for strategies to combat this debilitating disease. Future studies could explore specific inhibitors of mPGES-1 or EP receptors and their effects on MS progression and symptom management.

What research methods were used to investigate the relationship between microsomal prostaglandin E synthase-1 (mPGES-1) and Multiple Sclerosis, and what insights did they provide?

The study used an animal model of Multiple Sclerosis (MS) called experimental autoimmune encephalomyelitis (EAE) in mice. Researchers compared mice with normal microsomal prostaglandin E synthase-1 (mPGES-1) levels to mice genetically engineered to lack mPGES-1. This allowed them to observe the differences in disease progression and inflammation levels in the spinal cord, providing insights into the role of mPGES-1 in MS development. Further studies could investigate the effects of mPGES-1 in human cell cultures or clinical trials.