Introduction: Multiple sclerosis (MS), an autoimmune disease, attacks the
central nervous system, causing inflammation and damage. Diagnosed
in four forms, many clinically isolated syndrome (CIS) patients progress
to relapsing-remitting MS (RRMS). C1QA, a molecule linked to MS,
might be a treatment target due to its abnormal activity in the disease.
This study investigated mir-335-5p and its targeting C1QA expression
as potential biomarkers for disease progression. This relationship was
also evaluated from an epigenetic perspective between CIS, RRMS and
control groups.
Methods: Peripheral blood mononuclear cells (PBMCs) were isolated
from 18 CIS, 32 RRMS, and 16 control blood samples. RNA isolation and
Quantitative Real-Time PCR (qRT-PCR) were performed to detect the
expression levels of C1QA and miR-335-5p, while C1QA protein levels
were determined using ELISA.
Results: The data revealed significant increases in both C1QA gene
expression (p=0.0291) and miR-335-5p expression (p=0.0196) in CIS
patients compared to controls. Although increased expression levels were
observed for both parameters in RRMS patients versus controls, they
did not reach statistical significance. Patients with RRMS showed lower
levels of C1QA and miR-335-5p compared to those with CIS. Notably,
the decrease in miR-335-5p was statistically significant (p=0.0442). No
significant difference in C1QA protein levels was observed among the
groups (p >0.05).
Conclusion: miR-335-5p and C1QA emerge as potential biomarkers for
MS progression, exhibiting significant upregulation in CIS compared to
controls. miR-335-5p also shows significant downregulation in RRMS
compared to CIS. These findings support the potential of miR-335-5p
for distinguishing and understanding the progression of both CIS and
RRMS.
Keywords: C1QA, clinically isolated syndrome, expression, miR-335-5p,
relapsing-remitting multiple sclerosis