zahra samimi - Academia.edu (original) (raw)

Papers by zahra samimi

Investigating the correlation of the NF-κB and FoxP3 gene expression with the plasma levels of pro- and anti-inflammatory cytokines in rheumatoid arthritis patients

Clinical Rheumatology

Killer cell immunoglobulin-like receptors (KIRs) regulate the antitumor effect of Natural killer ... more Killer cell immunoglobulin-like receptors (KIRs) regulate the antitumor effect of Natural killer cells. This study aims to compare the frequency of KIR genes distribution in women with breast cancer and the control group in Kermanshah province. This study was performed on 53 women with BC and 37 healthy women. The KIR gene content was determined by polymerase chain reaction with sequence-specific primers (PCR-SSP). The frequency of the KIR- 2DL5B gene was significantly different between the two groups (P: 0.037), and this locus increases the risk of disease (OR: 2.491). The following results were associated with breast cancer risk: the cBx-tAtA distribution (OR: 5.122), the B content score 1 (OR: 5.122), tA01|tA01 (OR: 5.122) and inversely the following results were associated with protection: the cBx-tBx distribution (OR: 0.176), the B content score 2 (OR: 0.176), cA01|cB0X (OR: 0.287) and tA01|tB0X (OR: 0.301). These results suggested that KIR- 2DL5B, the cBx-tAtA, the B content s...

Intra-mPFC injection of sodium butyrate promotes BDNF expression and ameliorates extinction recall impairment in an experimental paradigm of post-traumatic stress disorder

Iranian Journal of Basic Medical Sciences, Sep 1, 2022

Increased autophagy in Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis patients

چهاردهمین کنگره بین المللی ایمونولوژی و آلرژی, 2018

The association between killer cell immunoglobulin-like receptor-ligand (KIR-L) and breast cancer risk among the Kermanshahi women

Meta Gene, 2022

Iranian Journal of Basic Medical Sciences, 2021

Objective(s): Treatments that reverse deficits in fear extinction are promising for the managemen... more Objective(s): Treatments that reverse deficits in fear extinction are promising for the management of post-traumatic stress disorder (PTSD). 5-Hydroxytryptamine type 3 (5-HT3) receptor is involved involved in the extinction of fear memories. The present work aims to investigate the role of 5HT3 receptors in the infralimbic part of the medial prefrontal cortex (IL-mPFC) in extinction of conditioned fear in the single prolonged stress (SPS) model of PTSD in rats. Materials and Methods: The effect of SPS administration was evaluated on the freezing behavior in contextual and cued fear conditioning models. After the behavioral tests, levels of 5HT3 transcription in IL-mPFC were also measured in the same animals using the real-time RT-PCR method. To evaluate the possible role of local 5HT3 receptors on fear extinction, conditioned freezing was evaluated in another cohort of animals that received local microinjections of ondansetron (a 5HT3 antagonist) and ondansetron plus a 5HT3 agonist ...

Brazilian Journal of Pharmaceutical Sciences, 2020

We performed this study to measure the Tumor Necrosis Factor-alpha (TNF-α) plasma level and to su... more We performed this study to measure the Tumor Necrosis Factor-alpha (TNF-α) plasma level and to survey its correlation with disease activity in the newly diagnosed Rheumatoid Arthritis (RA) patients and those who were under treatment with the combination of Disease-Modifying Anti-Rheumatic Drug (DMARD) plus Prednisolone (PSL).We enrolled 30 newly diagnosed RA patients who received no treatment regarding their disease, 30 patients under treatment with the combination of Methotrexate (MTX) + Hydroxychloroquine (HCQ) + PSL and 30 healthy subjects in this case-control study from September 2017 to December 2017. The level of plasma TNF-α was measured by enzyme-linked immunosorbent assay (ELISA) in each group. For assessment of disease severity, we used Disease Activity Score-28 (DAS-28) formula, and regarding DAS-28, we divided patients into four groups, including remission, low, moderate and high disease activity. There were no significant differences in the plasma level of TNF-α between the newly diagnosed RA patients and subjects who received MTX + HCQ + PSL, as well as healthy controls (p>0.05). There was a significant correlation between plasma levels of TNF-α and DAS-28 in the newly diagnosed patients with RA (r = 0.594, P = 0.001). Targeting TNF-α at the early stage of RA could have more beneficial effects on the amelioration of disease activity.

Scientific Journal of Kurdistan University of Medical Sciences, 2019

Background and Aim: Rheumatoid arthritis (RA) is an autoimmune inflammatory disease of unknown et... more Background and Aim: Rheumatoid arthritis (RA) is an autoimmune inflammatory disease of unknown etiology. The chemokines and their related receptors have a pivotal role in migration and homing of leukocyte involved in the pathogenesis of RA. The goal of this study was to measure the plasma levels of CCL-17 and CCL-25 and their receptors gene (CCR4 and CCR9) expression in rheumatoid arthritis patients. Materials and Methods: 30 untreated newly diagnosed and 30 under treatment RA patients with disease modifying anti-rheumatic drugs (DMARDs) as well as 30 healthy subjects participated in this study. We assessed the gene expression of CCR4 and CCR9 by the realtime PCR method, and measured plasma levels of CCL25 and CCL17 by enzyme-linked immunosorbent assay (ELISA). Results: Comparison between control group and newly diagnosed rheumatoid arthritis patients showed significantly lower expression of CCR4 and CCR9 (P=0.047, P=0.049 respectively) in the latter group. In addition, the plasma level of CCL-25 was significantly lower in both newly diagnosed and under treatment RA patients compared to that in the healthy subjects (P=0.017, P=0.030 respectively). Conclusion: The altered expression of chemokines and their related receptors, especially those involved in the leukocyte migration to the mucosa of the gastrointestinal tract may be associated with the pathogenesis of RA.

Immunological Investigations, 2020

Background: Rheumatoid arthritis (RA) is an autoinflammatory and self-perpetuating disease with b... more Background: Rheumatoid arthritis (RA) is an autoinflammatory and self-perpetuating disease with both articular and extra-articular manifestations, such as cardiovascular complications, which are the leading cause of mortality and morbidity in RA patients. Impaired sugar and lipid metabolism are considered as the critical risk factors for cardiovascular disease (CVD). Regarding the regulatory function of Raptor in the immunometabolism, in this study, we evaluated the association between plasma sugar and lipid profiles with the gene expression of Raptor and the cytokine tumor necrosis factor-α (TNF-α), as an inflammatory mediator, in peripheral blood leukocyte of RA patients. Material and methods: Thirty-five RA patients who received combinational disease modified anti-rheumatoid drugs (DMARD) regimen and thirty healthy subjects enrolled in this study. The gene expression of Raptor was assessed by the real-time PCR method, and the Plasma levels of glucose and lipids, as well as TNF-α, were obtained using Hitachi device and enzyme-linked immunosorbent assay (ELISA) technique, respectively. Results: The gene expression of Raptor was reduced significantly in RA patients compared to the healthy subjects (p = .001). The plasma level of HDL was significantly higher in RA patients than the control group (p = .001), while the plasma level of LDL was reduced significantly in these patients (p = .001). Conclusion: In our study, the reduced gene expression of Raptor may contribute to the impaired immunometabolism in RA patients, which is independent of plasma sugar and lipid profile.

Molecular Biology Reports, 2019

The disturbed immune homeostasis is involved in the pathogenesis of an array of autoimmune diseas... more The disturbed immune homeostasis is involved in the pathogenesis of an array of autoimmune diseases like rheumatoid arthritis (RA). The adenosine monophosphate-activated protein kinase (AMPK) with a pivotal role in immunometabolism process, also plays a regulatory function in the immune system. This study aims to evaluate the alteration of AMPK gene expression in peripheral blood leukocytes of RA patients and its effects on disease severity as well as plasma levels of antiinflammatory cytokines. 60 RA patients, including 30 newly diagnosed and 30 patients whose disease were under controlled with the combinational disease-modifying anti-rheumatic drug (DMARD), as well as 30 healthy subjects, were enrolled in our study. The gene expression of AMPK was evaluated using real-time PCR method. The plasma concentrations of IL-10 and TGF-β1 were measured using sandwich ELISA. The gene expression of AMPK was significantly lower in the newly diagnosed RA patients in comparison with the control group (P = 0.049). Inversely, in RA patients who received DMARD therapy, the gene expression of AMPK was significantly higher than the control group (P = 0.003). There was no significant correlation between AMPK gene expression and plasma levels of IL-10 and TGF-β1. The plasma levels of TGF-β1 was significantly higher in both newly diagnosed and under-treatment patients compared with healthy subjects (P < 0.001). The impaired gene expression of AMPK in peripheral blood leukocytes and elevated levels of plasma TGF-β1 can be contributed in RA pathogenesis.

Cell & Bioscience, 2019

Background: Autophagy is a catabolic process for degradation of intracellular components. Damaged... more Background: Autophagy is a catabolic process for degradation of intracellular components. Damaged proteins and organelles are engulfed in double-membrane vesicles ultimately fused with lysosomes. These vesicles, known as phagophores, develop to form autophagosomes. Encapsulated components are degraded after autophagosomes and lysosomes are fused. Autophagy clears denatured proteins and damaged organelles to produce macromolecules further reused by cells. This process is vital to cell homeostasis under both physiologic and pathologic conditions. Main body: While the role of autophagy in cancer is quite controversial, the majority of studies introduce it as an anti-tumorigenesis mechanism. There are evidences confirming this role of autophagy in cancer. Mutations and monoallelic deletions have been demonstrated in autophagy-related genes correlating with cancer promotion. Another pathway through which autophagy suppresses tumorigenesis is cell cycle. On the other hand, under hypoxia and starvation condition, tumors use angiogenesis to provide nutrients. Also, autophagy flux is highlighted in vessel cell biology and vasoactive substances secretion from endothelial cells. The matrix proteoglycans such as Decorin and Perlecan could also interfere with angiogenesis and autophagy signaling pathway in endothelial cells (ECs). It seems that the connection between autophagy and angiogenesis in the tumor microenvironment is very important in determining the fate of cancer cells. Conclusion: Matrix glycoproteins can regulate autophagy and angiogenesis linkage in tumor microenvironment. Also, finding details of how autophagy and angiogenesis correlate in cancer will help adopt more effective therapeutic approaches.

Clinical Rheumatology, 2019

Rheumatoid arthritis (RA) is the most common type of inflammatory arthritis leading to joint dama... more Rheumatoid arthritis (RA) is the most common type of inflammatory arthritis leading to joint damage and physical disability. Cardiovascular diseases (CVDs) are considered a common comorbidity in patients with RA. However, the mechanism underlying its pathogenesis is not definitively explained. Endothelial dysfunction caused by impaired nitric oxide synthesis is an early indicator of cardiovascular disease. Asymmetric and symmetric dimethylarginine (ADMA and SDMA, respectively) the inhibitors of endothelial nitric oxide synthase (NOS) have emerged as novel CVD risk factor determiners. Concerning the unmet need to identify a salutary biomarker for CVD prediction, the purpose of this meta-analysis was to assess the serum/plasma ADMA and SDMA levels in RA patients compared with the healthy controls. A thorough literature search was performed in PubMed, Scopus, Web of Science, and Google Scholar to identify all studies reporting ADMA and/or SDMA levels in RA patients compared with healthy controls. The quality of studies was evaluated using the Newcastle-Ottawa scale (NOS). Pooled standard mean difference (SMD) with 95% confidence interval (CI) was used as the effect size in this study. We also conducted stratified analysis based on assay methods and median age of the participants. Fourteen articles were included. The pooled serum/plasma levels of ADMA were higher in RA patients compared with those of healthy controls (SMD = 1.02, 95% CI = 0.49 to 1.55); However, no statistical differences between RA patients and healthy controls in serum/plasma SDMA levels was seen (SMD = 0.57, 95% CI = −0.21 to 1.36). Subgroup analyses suggested that participants aged > 50 years had higher levels of ADMA rather than controls and the measurement method was a source of heterogeneity for ADMA. According to the results of this metaanalysis, ADMA measurement but not SDMA, can be useful for assessment of endothelial dysfunction as a predictor of CVD risk in RA patients. Prospero registration number: CRD42019121126.

Immunological Investigations, 2019

Background: The effect of obesity on disease severity in rheumatoid arthritis (RA) remains contro... more Background: The effect of obesity on disease severity in rheumatoid arthritis (RA) remains controversial. Adipocytes secrete proinflammatory cytokines and adipokines which may contribute to RA disease activity. The goal of the present study is to address the association between body mass index (BMI) with plasma levels of leptin, pro-inflammatory cytokines, and RA disease severity. Methods: Fifty RA patients (20 newly diagnosed and 30 under treatment) as well as 30 age-and sex-matched healthy subjects were included in this survey. The plasma levels of leptin and proinflammatory cytokines, including TNF-α and IL-6, were measured, and the results were compared among the patients in the three different categories of BMI, including <25, ≥25-30, and ≥30. Results: In our study, a significant positive correlation was observed between disease activity score-28 (DAS-28) and BMI in overweight (OW) RA patients (p = .036 r = 0.440). The plasma levels of leptin were significantly higher in patients group, compared to healthy subjects (p < .05); moreover, leptin levels were significantly higher in OW and obese patients compared to RA patients with normal BMI (p = .011, p = .001, respectively) and also BMI had positive correlation with leptin concentrations just in the newly diagnosed patients (p < .0001, r = 0.748). There was no correlation between leptin and DAS-28. The plasma IL-6 and TNF-α did not show significant differences between RA patients and healthy subjects, and also the plasma leptin did not have any correlation with plasma levels of IL-6 and TNF-α. Conclusion: BMI contribution to RA disease severity is independent of systemic levels of leptin and pro-inflammatory cytokines.