Publications by authors named "Maryam Sadri"

6 Publications

  • Page 1 of 1

Association Between Vitamin D Receptor (VDR) and Vitamin D Binding Protein (VDBP) Genes Polymorphisms to Endometriosis Susceptibility in Iranian Women.

Reprod Sci 2021 May 4. Epub 2021 May 4.

Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Endometriosis is a chronic inflammatory disease that has been reported to be associated with immune system dysfunction. On the other hand, the effect of Vitamin D as an immune modulator and its relation with several autoimmune and inflammatory diseases has been previously investigated. Moreover, several studies have reported the polymorphisms of VDR and VDBP genes can change the functions of these molecules. Therefore, these polymorphisms may be influential on endometriosis pathogenesis. In this study, we aimed at evaluating the association between VDR gene (FokI (F/f), BsmI (B/b), ApaI (A/a), TaqI (T/t)), and VDBP gene (GC*1S, GC*1F, and GC*2) polymorphisms with endometriosis in Iranian women population. This case-control study was performed on 120 women with endometriosis and 110 healthy women. ARMS-PCR and PCR-RFLP methods were used to inspect polymorphisms in VDR and VDBP genes, respectively. Based on the results, there was no statistically significant difference between the cases with endometriosis and control subjects in terms of genotypes and allele frequencies of VDR and VDBP gene polymorphisms. These data suggest that VDR and VDBP gene polymorphisms may have no role in endometriosis susceptibility in Iranian women.
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http://dx.doi.org/10.1007/s43032-021-00598-zDOI Listing
May 2021

Overexpression of bHLH domain of HIF-1 failed to inhibit the HIF-1 transcriptional activity in hypoxia.

Biol Res 2020 Jun 5;53(1):25. Epub 2020 Jun 5.

Immunology Research Center, Iran University of Medical Sciences, Tehran, Iran.

Background: Hypoxia inducible factor-1 (HIF-1) is considered as the most activated transcriptional factor in response to low oxygen level or hypoxia. HIF-1 binds the hypoxia response element (HRE) sequence in the promoter of different genes, mainly through the bHLH domain and activates the transcription of genes, especially those involved in angiogenesis and EMT. Considering the critical role of bHLH in binding HIF-1 to the HRE sequence, we hypothesized that bHLH could be a promising candidate to be targeted in hypoxia condition.

Methods: We inserted an inhibitory bHLH (ibHLH) domain in a pIRES2-EGFP vector and transfected HEK293T cells with either the control vector or the designed construct. The ibHLH domain consisted of bHLH domains of both HIF-1a and Arnt, capable of competing with HIF-1 in binding to HRE sequences. The transfected cells were then treated with 200 µM of cobalt chloride (CoCl) for 48 h to induce hypoxia. Real-time PCR and western blot were performed to evaluate the effect of ibHLH on the genes and proteins involved in angiogenesis and EMT.

Results: Hypoxia was successfully induced in the HEK293T cell line as the gene expression of VEGF, vimentin, and β-catenin were significantly increased after treatment of untransfected HEK293T cells with 200 µM CoCl. The gene expression of VEGF, vimentin, and β-catenin and protein level of β-catenin were significantly decreased in the cells transfected with either control or ibHLH vectors in hypoxia. However, ibHLH failed to be effective on these genes and the protein level of β-catenin, when compared to the control vector. We also observed that overexpression of ibHLH had more inhibitory effect on gene and protein expression of N-cadherin compared to the control vector. However, it was not statistically significant.

Conclusion: bHLH has been reported to be an important domain involved in the DNA binding activity of HIF. However, we found that targeting this domain is not sufficient to inhibit the endogenous HIF-1 transcriptional activity. Further studies about the function of critical domains of HIF-1 are necessary for developing a specific HIF-1 inhibitor.
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http://dx.doi.org/10.1186/s40659-020-00293-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275393PMC
June 2020

IL-10 induces TGF-β secretion, TGF-β receptor II upregulation, and IgA secretion in B cells.

Eur Cytokine Netw 2019 09;30(3):107-113

Tehran University of Medical Sciences, Pediatrics Center of Excellence, Children's Medical Center, Research Center for Immunodeficiencies, Tehran, Iran.

Interleukin-10 (IL-10) is a pleiotropic cytokine, which has both regulatory and stimulatory effects on different immune cell types. Different studies have reported the importance of IL-10 and Transforming growth factor-beta (TGF-β) in the regulation of B cell class switching the production of immunoglobulin A (IgA); however, the underlying mechanisms remain to be fully elucidated. The objective of this study was to investigate the TGF-β response during B stimulation of human B cells by IL-10. Pan B cells of healthy donors were negatively purified by a magnetic cell separation technique. B cells were cultured with multimeric CD40 ligand (mCD40L) and IL-10 for two and seven days. After harvesting in specific days, TGF-β receptor II and surface IgA expression was determined by flow cytometry, while IgA and TGF-β secretion was assessed by enzyme-linked immunosorbent assay. B cells endogenously expressed TGF-β receptor II and after 48 hours cultivation with mCD40L or mCD40L plus IL-10, both the expression of this receptor and the production of TGF-β were significantly increased. Notably, TGF-β levels following stimulation with mCD40L and IL-10 were higher than those produced by B cells stimulated with mCD40L alone. Furthermore, at day 7 and following IL-10 stimulation, there was a significant rise in the amount of IgA secretion by class-switched plasma cells, which was higher than stimulation with mCD40L alone. Our findings suggest that IL-10 can modulate TGF-β production and TGF-β receptor expression in mCD40-activated human B lymphocytes.
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http://dx.doi.org/10.1684/ecn.2019.0434DOI Listing
September 2019

Association between +4259 T>G and -574 G>T Polymorphisms of TIM-3 with Asthma in an Iranian Population.

Iran J Allergy Asthma Immunol 2017 Aug;16(4):321-328

Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

T-cell immunoglobulin and mucin domain (TIM)-3 have been shown to negatively regulate Th1 cell-mediated immunity. Activation of TIM-3 by galectin-9 induces Th1 cell apoptosis, which may contribute to skewing of immune response towards Th2-dominant immunity. The aim of this study was to determine whether certain genetic variations of TIM-3 influence predisposition to asthma in a sample of Iranian population. This case-control study was conducted on 209 patients with asthma and 200 healthy controls. The +4259 T>G and -574 G>T polymorphisms were detected using polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) and amplification refractory mutation system-PCR(ARMS-PCR). Total serum IgE was further measured with ELISA. Notably, +4259T > G and-574G>T polymorphisms of TIM-3 were significantly associated with the susceptibility to asthma. In addition, the present study showed a significant difference between the distribution frequency of the GT + TT genotype and T allele on the +4259 T>G and -574 G>T locus between the groups.However, no correlation between the +4259 T > G and -574G > T polymorphisms and total serum IgE levels were observed. Together these results suggest that the TIM-3 +4259 T>G and -574 G>T polymorphisms are greatly associated with the susceptibility of Iranian population to asthma, which could open up new horizons for  better understanding of the pathophysiology, diagnostic, prognostic and therapeutic approaches of asthma.
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August 2017

Static Magnetic Field Effect on Cell Alignment, Growth, and Differentiation in Human Cord-Derived Mesenchymal Stem Cells.

Cell Mol Bioeng 2017 Jun 20;10(3):249-262. Epub 2017 Mar 20.

4Department of Stem Cells and Developmental Biology at Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.

This investigation is performed to evaluate the impact of static magnetic field on the Cell growth alignment, and differentiation potential in Human Mesenchymal Stem cells derived from human newborn cords. -cultured mesenchymal stem cells derived from human newborn cords were exposed to SMF up to 24 mT and compared with the control (unexposed) cultures. Viability was assessed Trypan Blue staining and MTT assay. Cell cycle progression was studied after flow cytometry data analysis. Sox-2, Nanong, and Oct-4 Primers used for RT-PCR experiment. Morphological studies showed that the exposed cells were significantly aligned in parallel bundles in a correlation with the magnetic field lines. Viability measurements showed a significant reduction in cell viability which was noted after exposure to static magnetic field and initiated 36 h after the end of exposure time. Flow cytometric data analysis confirmed a decrease in G1 phase cell population within the treated and cultured groups compared with the corresponding control samples. However, the induced changes were recovered in the cell cultures after the post-exposure culture recovery time which may be attributed to the cellular repair mechanisms. Furthermore, the proliferation rate and Oct-4 gene expression were reduced due to the 18 mT static magnetic field exposure. The significant proliferation rate decrease accompanied by the Sox-2, Nanong, and Oct-4 gene expression decline, suggested the differentiation inducing effects of SMF exposure. Exposure to Static Magnetic fields up to 24 mT affects mesenchymal stem cell alignment and proliferation rate as well as mRNA expression of Sox-2, Nanong, and Oct-4 genes, therefore can be considered as a new differentiation inducer in addition to the other stimulators.
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http://dx.doi.org/10.1007/s12195-017-0482-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6816594PMC
June 2017