|Downregulation of Autophagy-related Genes in Macrophages from Patients with Behcet's Disease|
|Mahdi Mahmoudi1, Mohammad Taghi Palizgir1, Maryam Akhtari2, Farhad Shahram1, Shayan Mostafaei1, Maassoomeh Akhlaghi1, Soheila Sobhani1|
|1Tehran University of Medical Sciences, Rheumatology Research Center, Tehran, Iran, Islamic Republic Of
2Department of Cell and Molecular Biology, Tehran University of Medical Sciences, Tehran, Iran
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Keywords : Behcet's disease, autophagy-related genes, macrophage, inflammation
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Objectives: Overwhelming chemokine and inflammatory cytokines characterize the immunological profile and inflammatory settings of Behcet's disease (BD). The connection between autophagy-related genes (ATGs) and various perspectives of innate and adaptive immunobiology, such as antigen presentation, immune tolerance, lymphocyte development and differentiation, cytokine signaling, and inflammation have been implicated. The aim of this study was to evaluate the mRNA expression profile of ATGs in macrophages of patients with BD.
Materials and methods: Whole bloodsampleswere obtained from 10 BD patients and 10 healthy controls. Monocytes were isolated from the blood samples and then differentiated to macrophages using macrophage-colony stimulating factor (M-CSF). After total RNA extraction and cDNA synthesis, quantification analysis of ATGs, including ATG5, ATG7, ATG12, LC3b, mTOR, RAPTOR, and RICTOR, was conducted by SYBR Green master mix and real-time PCR.
Results: mRNA expression of all ATGs was downregulated in macrophages of BD patients compared with healthy controls. Of note, there were statistically significant downregulation of ATG12 and LC3b mRNAs in macrophages of BD patients in comparison to that of healthy control group (P= 0.007 and 0.021, respectively).
Conclusions: Considering the role of autophagy in initiation of immune responses and then clearance of dead cells as well as its participation in the development and differentiation of immune cells, downregulation of ATGs in macrophages of BD patients may be involved in uncontrolled immune response and overproduction of inflammatory cytokines.
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