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Molavi, O.

Publications and source records attributed to Molavi, O..

3 recordsLinked to original sources

Growth inhibitory effect of cerebrospinal fluid of multiple sclerosis patients on HFF2 cells

Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination of the central nervous system (CNS). Occurrence of immunogenic cell death (ICD) in this disease and expression of ICD markers in the CSF of MS patients are documented. However, cytotoxic effect of MS patients cerebrospinal fluid (CSF) on the cells is not reported. To evaluate the cytotoxic impact of CSF from MS patients on cell viability, human foreskin fibroblast (HFF2) cells were treated with CSF samples from individuals with MS and healthy controls. The results inferred that patient-derived CSF significantly declined the survival of HFF2 cells in comparison to the CSF of healthy individuals. This observation implies a cytotoxic environment and characteristic of patients CSF, which could be due to the presence of cellular-damaging factors such as calreticulin (CRT) in the patients CSF. The cytotoxic environment of CSF might reflect ICD occurrence in CNS of the patients and also could explain the progressive essence of the disease.

neuroscience↗

Annexin A1, Calreticulin and High Mobility Group Box 1 are elevated in Secondary Progressive Multiple Sclerosis: Does Immunogenic Cell Death Occur in Multiple Sclerosis?

Multiple sclerosis (MS) is a chronic neuroinflammatory diseases characterized by demyelination of the nerve fibers. Immunogenic cell death (ICD) is a process, during which damaged and stressed cells release danger-associated molecular patterns (DAMPs) activating immune responses. This study aimed to elucidate the induction of ICD in MS diseases. To achieve this goal, the level of DAMPs including Annexin A1, calreticulin and HMGB1 was measured in the cerebrospinal fluid (CSF) of a secondary progressive multiple sclerosis (SPMS) patient in comparison to control group. Results showed significant upregulation (more than two- fold) of Annexin A1, calreticulin and HMGB1 in the CSF of the patient. Although further studies are suggested in this regard, this data could imply induction of ICD in MS. The proposed ICD might trigger immune response against neural cells resulting in neuroinflammation and demyelination in CNS in MS. Our observation could suggest inclusion of ICD interfering treatments in routine MS therapy.

immunology↗

Epstein-Barr virus-encoded BART9 and BART15 miRNAs are elevated in exosomes of cerebrospinal fluid from relapsing-remitting multiple sclerosis patients

Epstein-Barr virus (EBV) infection is approved as the main environmental trigger of multiple sclerosis (MS). In this path, we quantified EBV-encoded BART9-3p and BART15 miRNAs in exosomes of cerebrospinal fluid (CSF) of untreated relapsing-remitting MS (RRMS) patients in comparison with the control group. Interestingly, patients displayed significant upregulation of BART9-3p (18.4-fold) and BART15 (3.1-fold) expression in CSF exosomes. Moreover, the expression levels of miR-21-5p and miR-146a-5p were found to be significantly elevated in the CSF samples obtained from the patient group in comparison to those obtained from the HC group. The levels of Interferon gamma (IFN-{gamma}), interleukin-1{beta} (IL-1{beta}), interleukin- 6 (IL-6), interleukin-17 (IL-17), interleukin-23 (IL-23), transforming growth factor beta (TGF- {beta}), and tumor necrosis factor alpha (TNF-) were observed to be significantly elevated in the serum and CSF exosomes of the patients. The highest increase was observed in TGF-{beta} (8.5- fold), followed by IL-23 (3.9-fold) in CSF exosomes. These findings are in agreement with the association between EBV infection and inflammatory cytokines induction. Furthermore, the ratios of TGF-{beta}:TNF- and TGF-{beta}:IFN-{gamma} attained values of 4 to 16.4 and 1.3 to 3.6, respectively, in the CSF exosomes of the patients, in comparison to those of the control group. Remarkable stimulation of EBV BART9-3p, BART15 miRNAs, and inflammatory cytokines expression in CSF exosomes confers a substantial link between EBV in MS onset and also the infection-to-MS transition.

molecular biology↗