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Updated: Nov 29, 2025

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
Published on: May 2, 2025
CCN3 is dynamically regulated by treatment and disease state in multiple sclerosis
Michelle Naughton1, Jill Moffat1, George Eleftheriadis1
1Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, 97 Lisburn Road, Belfast, Northern Ireland, BT9 7BL, UK.
CCN3 levels in multiple sclerosis (MS) patients varied by disease state and treatment, correlating with cerebrospinal fluid (CSF) and immune cells, suggesting a role in neuroinflammation.
Area of Science:
- Neuroimmunology
- Central Nervous System (CNS) Disorders
- Myelin Biology
Background:
- Multiple sclerosis (MS) is an immune-mediated CNS disease causing myelin damage.
- CCN3 is implicated in immune function and myelin repair.
- This study profiles CCN3 in MS disease states and treatments.
Purpose of the Study:
- To comprehensively profile CCN3 expression in multiple sclerosis.
- To investigate CCN3's role in relation to MS disease state and treatment.
- To explore CCN3's presence and distribution within the CNS.
Main Methods:
- Analyzed CCN3 expression in plasma, immune cells (PBMCs, CD4+ T cells), CSF, and brain tissue.
- Utilized techniques including ELISA, Western blot, qPCR, histology, and in situ hybridization.
- Compared MS patients (progressive, relapsing-remitting) with controls and other neurological conditions.
Main Results:
- Plasma CCN3 levels were similar between MS patients and controls but higher in progressive MS and with interferon-β treatment versus natalizumab.
- A positive correlation between plasma and CSF CCN3 levels was observed in MS patients.
- CCN3 mRNA was upregulated in PBMCs and CD4+ T cells of MS patients; CNS expression varied in different tissue types.
Conclusions:
- This study presents the first extensive profile of CCN3 in MS.
- Findings suggest CCN3 may play a role in neuroimmunological functions within the CNS.
- Further research is warranted to elucidate CCN3's specific contributions to MS pathogenesis.
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