Resolvin D1 (Rvd1) Attenuates LPS-Stimulated Inflammation Through Downregulation of miR-155, miR -146, miR -148 and Krupple Like Factor 5.

Background: Chronic inflammation is associated with many inflammatory diseases. Specialized pro-resolving mediators (SPMs) are well known for their crucial role in promoting the resolution phase of inflammation and restoring tissue homeostasis. Resolvin D1 (RvD1) is an endogenous omega-3-derived lipid mediator with pro-resolving activity.

Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases.

Nowadays, it is well recognized that apoptosis, as a highly regulated cellular process, plays a crucial role in various biological processes, such as cell differentiation. Dysregulation of apoptosis is strongly implicated in the pathophysiology of numerous disorders, making it essential to comprehend its underlying mechanisms. One key factor that has garnered significant attention in the regulation of apoptotic pathways is HMG-CoA reductase degradation protein 1, also known as HRD1.

Association of Rs7217186 Polymorphism of Arachidonic Acid 15-Lipoxygenase (ALOX15) Gene with Susceptibility to Allergic Rhinitis.

Background: Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa, caused by exposure to environmental allergens. It is known that 15-lipoxygenase (15-LOX) is involved in the biosynthetic pathways of anti-inflammatory lipid mediators, including resolvins and protectins.

Methods: In this study, which was performed on 130 AR patients and 130 healthy controls, we aimed to investigate the association of susceptibility to AR with two selected single-nucleotide polymorphisms (SNPs), that is, rs2619112:A>G and rs7217186:C>T, in the intron regions of arachidonic acid 15-LOX () gene, using SNPinfo and Regulome DB tools.

Overexpression of Synoviolin and miR-125a-5p, miR-19b-3p in peripheral blood of rheumatoid arthritis patients after treatment with conventional DMARDs and methylprednisolone.

Purpose: SYVN1 is an endoplasmic reticulum (ER)-resident E3 ubiquitin ligase that has an essential function along with SEL1L in rheumatoid arthritis (RA) pathogenesis. This study aimed to investigate the changes in the expression of peripheral blood ncRNAs and SYVN1-SEL1L affected by DMARDs treatment.

Methods: Twenty-five newly diagnosed RA patients were randomly assigned to receive conventional DMARDs (csDMARDs) and methylprednisolone for six months.

Association of Single Nucleotide Polymorphisms (SNPs) of Chemoattractant Receptor23 (ChemR23) Gene with Susceptibility to Allergic Rhinitis.

The chemoattractant Receptor23 (ChemR23) plays an essential role in triggering and resolving acute inflammation. This study aimed to evaluate the association between four potentially functional SNPs of the chemR23 gene (rs4373981 G > C, rs73201532 C > T, rs35121177 G > A, and rs4964676 G > A) with susceptibility to Allergic rhinitis (AR). 130 patients with allergic rhinitis and 130 healthy individuals were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.

Imbalanced serum levels of resolvin E1 (RvE1) and leukotriene B4 (LTB4) may contribute to the pathogenesis of atherosclerosis.

Persistent and chronic unresolved inflammation exerts a critical role in developing atherosclerosis; however, mechanisms that prevent the resolution of inflammation in atherosclerosis are poorly delineated. This study aims to evaluate the serum levels of inflammatory high-sensitivity C-reactive protein (hsCRP), pro-inflammatory leukotriene B4 (LTB4), besides anti-inflammatory compounds, including eicosapentaenoic acid (EPA) and its derivative resolvin E1 (RvE1) in patients with atherosclerosis. Thirty-four atherosclerosis patients and thirty-two age- and sex-matched healthy individuals were included in this study.

Association of IFIH1 and DDX58 genes polymorphism with susceptibility to COVID-19.

Pattern recognition receptors of the innate immune system, such as RIG-I and MDA5, are responsible for recognizing viruses and inducing interferon production. Genetic polymorphisms in the coding regions of RLR may be associated with the severity of COVID-19. Considering the contribution of the RLR signaling in immune-mediated reactions, this study investigated the association between three SNP in the coding region of IFIH1 and DDX58 genes with the susceptibility to COVID-19 in the Kermanshah population, Iran.

Association of ANRIL Gene Single-Nucleotide Polymorphisms With Allergic Rhinitis in Kurdish Population From Kermanshah, Iran.

Background: Allergic rhinitis (AR) is the most common inflammatory disorder of the upper airway caused by aberrant immune responses to allergens in genetically predisposed individuals. Recently, the long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) has been identified as a novel genetic factor associated with increased AR risk.

Objectives: This study aimed to evaluate the potential correlation of gene single nucleotide polymorphisms (SNPs) with AR risk in the Kurdish population of Kermanshah, Iran.

Co-treatment with Fexofenadine and Budesonide Increases FoxP3 Gene Expression in Patients with Allergic Rhinitis.

Background: T helper type 2 (Th2), Th17, and regulatory T cells (Tregs) play essential roles in the pathogenesis and control of allergic rhinitis (AR). Fexofenadine and budesonide are first-line treatments for AR. This study aimed to investigate the effect of co-treatment with fexofenadine and budesonide on the expression of Th2, Th17, and Treg-specific transcription factors (GATA-binding protein 3 [GATA-3], RAR-related orphan receptor gamma [RORγt], and forkhead box P3 [FoxP3], respectively) in AR patients.

Inhibition of ERAP1 represses HLA-B27 free heavy chains expression on polarized macrophages and interrupts NK cells activation and function from ankylosing spondylitis.

Background: We aimed to assess if Endoplasmic reticulum aminopeptidase 1 (ERAP1) polymorphisms might impress Human leukocyte antigen (HLA)-B27-free heavy chains (FHCs) expression on macrophages and eventually NK cell activation in Ankylosing spondylitis (AS).

Methods: Blood samples were obtained from 10 HLAB27 patients with protective and 10 HLAB27 patients with non-protective genotype. Monocytes were isolated and polarized toward M1 and M2 macrophages.

MicroRNAs-mediated regulation pathways in rheumatic diseases.

Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are two common rheumatic disorders marked by persistent inflammatory joint disease. Patients with RA have osteodestructive symptoms, but those with AS have osteoproliferative manifestations. Ligaments, joints, tendons, bones, and muscles are all affected by rheumatic disorders.

Dysregulation of Long Noncoding RNA NEAT1/miR-199a-5/BiP Axis in Patients with Diabetic Neuropathy.

Objective: Diabetic neuropathy (DN) is a type of nerve damage and the most common complication of diabetes. Regarding the association between endoplasmic reticulum (ER) stress with the pathogenesis of neuropathy, this study aims to examine binding immunoglobulin protein (BiP) gene expression and long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1), miR-199a-5 as its regulator in the peripheral blood of DN patients compared to diabetic patients without neuropathy.

Methods: Peripheral blood samples were obtained from DN (n = 20) patients and diabetic patients without neuropathy (non-DN) (n = 20).

Efficacy of DMARDs and methylprednisolone treatment on the gene expression levels of HSPA5, MMD, and non-coding RNAs MALAT1, H19, miR-199a-5p, and miR-1-3p, in patients with rheumatoid arthritis.

Background: Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by joint damage and even extra-articular involvement. In this study, the gene expression levels of MALAT1, H19 and their possible downstream microRNAs, miR-199a-5p, miR-1-3p, and the predicted targets of these miRNAs, HSPA5 and MMD, were examined.

Methods: Twenty-five newly diagnosed RA patients and 25 healthy individuals were included.

HRD1 in human malignant neoplasms: Molecular mechanisms and novel therapeutic strategy for cancer.

In tumor cells, the endoplasmic reticulum (ER) plays an essential role in maintaining cellular proteostasis by stimulating unfolded protein response (UPR) underlying stress conditions. ER-associated degradation (ERAD) is a critical pathway of the UPR to protect cells from ER stress-induced apoptosis and the elimination of unfolded or misfolded proteins by the ubiquitin-proteasome system (UPS). 3-Hydroxy-3-methylglutaryl reductase degradation (HRD1) as an E3 ubiquitin ligase plays an essential role in the ubiquitination and dislocation of misfolded protein in ERAD.

Evaluation of the relationship between IL-6 gene single nucleotide polymorphisms and the severity of COVID-19 in an Iranian population.

Background: Emerged coronavirus disease 2019 (COVID-19) is a pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2). Disease severity is associated with elevated levels of proinflammatory cytokines, such as interleukin-6 (IL-6). Genetic polymorphisms in the regulatory regions of cytokine genes may be associated with differential cytokine production in COVID-19 patients.

The MALAT1-H19/miR-19b-3p axis can be a fingerprint for diabetic neuropathy.

Background: Diabetic neuropathy (DN) is one of the most common microvascular complications of diabetes that is attributed to impaired immune regulation. In this study, we first examined the expression of long non-coding (lncRNAs) MALAT1 and H19, and their downstream microRNAs (miRNAs) miR-19b-3p, miR-125a-5p, and then assayed the mRNA expression of downstream targets of these miRNAs, including SEMA4C, SEMA4D, PLXNB2, ATG14, and ATG16L1.

Methods: Peripheral blood samples were obtained from 20 DN patients, 20 diabetic patients without neuropathy (non-DN), and 10 healthy controls (HC).

The axis of long non-coding RNA MALAT1/miR-1-3p/CXCR4 is dysregulated in patients with diabetic neuropathy.

Background: Diabetic neuropathy (DN) is a prevalent complication of diabetes mellitus characterized by pain and inflammation. Long non-coding RNAs (lncRNAs) have been associated with DN. This study aimed to investigate transcript levels of Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), microRNA (miR)-1-3p, and C-X-C motif chemokine receptor 4 (CXCR4) in the DN patients and type 2 diabetes mellitus (T2DM) cases without neuropathy.

Upregulation of Unfolded Protein Response and ER Stress-Related IL-23 Production in M1 Macrophages from Ankylosing Spondylitis Patients.

The inflammatory interleukin (IL)-23/IL-17 axis plays an important role in the pathogenesis of ankylosing spondylitis (AS), but with an unknown regulatory mechanism. This study aimed to investigate the role of endoplasmic reticulum (ER) stress and autophagy pathway in the expression of IL-23 in peripheral blood-derived macrophages in AS patients. Peripheral blood samples were obtained from 15 AS and 15 healthy control subjects.

The effect of treatment with fexofenadine and fluticasone propionate on the gene expression levels of Th9 transcription factors in patients with allergic rhinitis.

T helper-9 (Th9) is a new T cell subset involved in allergic rhinitis (AR) pathogenesis. Fexofenadine and fluticasone propionate are the first effective line of AR treatment. This study aimed to evaluate the effect of fexofenadine and fluticasone propionate on the gene expression levels of Interferon regulatory factor 4 (IRF4), B cell-activating transcription factor-like (BATF), and SPI1 gene-encoded protein (PU.

A comprehensive in Silico analysis of the functional and structural impact of single nucleotide polymorphisms (SNPs) in the human IL-33 gene.

Interleukin 33 (IL-33) is the latest member of the IL-1 cytokine family, which plays both pro - and anti-inflammatory functions. Numerous Single-nucleotide polymorphisms (SNPs) in the IL-33 gene have been recognized to be associated with a vast variety of inflammatory disorders. SNPs associated studies have become a crucial approach in uncovering the genetic background of human diseases.

Retinoic Acid Correlates with Reduced Serum IL-10 And TGF-β in Allergic Rhinitis.

Background: Retinoic acid (RA) plays a key role in naïve T cell differentiation into FOXP3+ Treg cell in the respiratory airways. The present study aims to investigate RA and Treg-related cytokine serum levels, salivary IgA levels, FOXP3 and IL-4 gene expression, and the relationships between RA serum levels and Treg-related cytokines in allergic rhinitis (AR) patients and healthy controls.

Methods: Salivary IgA and serum IgE, RA, IL-10, and TGF-β concentrations were measured by ELISA in 37 AR patients and 30 age- and sex-matched healthy controls.

Association of interleukin-12B rs6887695 with susceptibility to allergic rhinitis.

Interleukin-12 (IL-12) is a heterodimeric cytokine encoded by two separate genes, IL12A and IL12B, which may play a regulatory role in allergen-induced inflammation through CD4 T-cell subsets polarization. The aim of this study was to investigate the association of single-nucleotide polymorphisms (SNPs) in the IL12B gene with susceptibility to allergic rhinitis (AR). We performed a case-control study including 130 AR patients and 130 healthy controls to evaluate the possible association between IL12B gene SNPs (rs3212227, rs6887695) and the risk of AR using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.

Determination of the transcriptional level of long non-coding RNA NEAT-1, downstream target microRNAs, and genes targeted by microRNAs in diabetic neuropathy patients.

Background: Diabetic neuropathy (DN) is one of the microvascular complications of diabetes that leads to peripheral sensorimotor and autonomic nervous system damages. In this study, we first examined the expression of lncRNA NEAT-1 and its downstream microRNAs, miR-183-5p, miR-433-3p, and then examined mRNA expression of ITGA4, ITGB1, SESN1, and SESN3 as the downstream targets of miR-183-5p, miR-433-3p.

Methods: The blood sample was obtained from a total of 40 patients with type 2 diabetes (20 DN patients and 20 non-DN diabetic cases) and ten healthy individuals.