STAT5a and STAT6 gene expression levels in multiple sclerosis patients

Mahsa Hatami1, Tayyebali Salmani1, Shahram Arsang-Jang2

  • 1Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Cytokine
|November 12, 2017
PubMed

Insights

STAT5a gene expression is down-regulated and STAT6 gene expression is up-regulated in multiple sclerosis (MS) patients, suggesting their role in immune response imbalance in MS.

Area of Science:

  • Neuroimmunology
  • Molecular Biology

Background:

  • Multiple sclerosis (MS) is an autoimmune CNS disease characterized by inflammation.
  • Cytokines and the Janus kinase/signal transducers and activators of transcriptions (JAK/STAT) pathway are implicated in MS pathogenesis.
  • Dysregulation of the JAK/STAT pathway is linked to adverse pathological outcomes in MS.

Purpose of the Study:

  • To compare the expression levels of STAT5a and STAT6 genes in relapsing-remitting MS (RR-MS) patients and healthy controls.
  • To investigate the correlation between STAT5a and STAT6 gene expression and clinical parameters in MS patients.

Main Methods:

  • Blood samples were collected from 50 RR-MS patients and 50 healthy controls.
  • Taqman Quantitative Real-Time PCR was used to measure STAT5a and STAT6 gene expression.
  • Correlation analysis was performed between gene expression and the Kurtzke Expanded Disability Status Scale (EDSS).

Main Results:

  • STAT5a gene expression was significantly down-regulated in MS patients compared to controls (p = .049).
  • STAT6 gene expression was significantly up-regulated in MS patients compared to controls (p = .046).
  • STAT6 expression correlated significantly with EDSS scores, while STAT5a expression did not correlate with clinical findings or STAT6 expression.

Conclusions:

  • STAT5a and STAT6 gene dysregulation may contribute to immune response imbalance in MS.
  • Further research is needed to elucidate the precise mechanisms and potential of STAT5a and STAT6 as biomarkers for MS.

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