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    <responseDate>2026-10-15T06:41:52Z</responseDate>
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            <header>
                <identifier>oai:data.mendeley.com/2gtcvmf4t2.1</identifier>
                <datestamp>2023-08-03T02:51:36Z</datestamp>
            </header>
            <metadata><oai_dc:dc xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <dc:creator>Inostroza-Nieves, Yaritza</dc:creator>
    <dc:title>Endothelin-1 as an Activator of Pro-inflammatory Microglia Cells in Multiple Sclerosis</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>Background: Multiple sclerosis (MS) is a neurodegenerative autoimmune disease characterized by inflammation, demyelination, and axonal degeneration. In MS patients, demyelination is associated with activated microglia. ET-1 is a potent vasoconstrictor that has been documented in MS. However, the mechanism of how ET-1 activates a proinflammatory response is unknown. 

Objective: Demonstrate that high levels of ET-1 contribute to the progression of MS.

Methods: C57BL/6 mice were used with or without induced experimental autoimmune encephalomyelitis (EAE). The brain ET-1 levels were measured by qPCR and ELISA. HMC3 cells were treated with ET-1 in the presence or absence of endothelin receptor B antagonist, BQ788. Nitric Oxide (NO) and ROS were measured using Griess Reagent and MUSE Oxidative Stress kit.

Results: ET-1 was upregulated in EAE mice. ET-1 levels were correlated with EAE score at onset. ET-1 increases TNF levels in HMC3 cells, and it was decreased by the BQ788. iNOS, NO, and ROS production are induced by ET-1 in HMC3 cells, and treatment with BQ788 decreases them.

Conclusion: These data suggest that ET-1 was able to activate microglia, increasing inflammatory cytokines, NO, and ROS. This is a novel mechanism of microglial cell activation and will provide key information to understand MS pathogenesis.
</dc:description>
    <dc:subject>Microglia</dc:subject>
    <dc:subject>Endothelin</dc:subject>
    <dc:subject>Multiple Sclerosis</dc:subject>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/2gtcvmf4t2.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/2gtcvmf4t2.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
    <dc:rights>http://creativecommons.org/licenses/by/4.0</dc:rights>
    <dc:relation>https://data.mendeley.com/datasets/2gtcvmf4t2</dc:relation>
    <dc:date>2023-08-03T02:51:36Z</dc:date>
</oai_dc:dc></metadata>
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