Transcriptional activity of genes-encoding kinin B1 and B2 receptors and kinin-dependent genes in nasal polyps

Rostkowska-Nadolska, Beata; Kapral, Małgorzata; Frączek, Marcin; Kowalczyk, Małgorzata; Gawron, Wojciech; Mazurek, Urszula

doi:10.2478/v10039-009-0045-0

Cited by 9 publications

(16 citation statements)

References 28 publications

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“…In addition, BR2 expression was demonstrated in peripheral nerve fibers, whereas BR1 expression was not observed in nerves (59). The mRNA expression of BR1 and BR2 in eosinophilic CRSwNP was significantly higher than in normal mucosa (60), suggesting the role of BK and its receptors in the etiology of NPs, where a low expression of TGF-b1 was also detected (61). However, further study is needed to determine whether there is a cross-talk.…”

Section: Other Pathwaysmentioning

confidence: 99%

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Yang

Zhang

Feng

et al. 2014

Allergy

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Transforming growth factor-beta 1 (TGF-b1) has been reported being involved in the remodeling and immunosuppression processes of inflammatory airway diseases; understanding the regulation of TGF-b1 is therefore a key to unravel the pathomechanisms of these diseases. This review briefly summarizes the current knowledge on the influencing factors for driving TGF-b1 and its regulatory pathways in inflammatory airway diseases and discusses possible therapeutic approaches to TGF-b1 control. The factors include smoking and oxidative stress, prostaglandins (PGs), leukotrienes (LTs), bradykinin (BK), and microRNAs (miRs). Based on the summary, new innovative treatment strategies may be developed for inflammatory airway diseases with an impaired expression of TGF-b1.The transforming growth factor-beta (TGF-b) superfamily is critically involved in embryonic development, organogenesis, and tissue homeostasis. It acts as multifunctional regulators of cell growth and differentiation and consists of more than 40 members, mainly including TGF-bs, bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), activins, and inhibins. Between these superfamily members, there is a complex network of regulatory mechanisms (1, 2).Possessing immunomodulatory and fibrogenic characteristics, TGF-b1 is a pleiotropic and multifunctional cytokine secreted from various types of cells, such as endothelial, epithelial and smooth muscle cells, as well as fibroblasts and most immune system cells.Transforming growth factor-beta 1 regulation is unique because it is targeted to the extracellular matrix as a biologically inactive complex, which consists of a mature 25-kDa polypeptide dimer (TGF-b), a latency-associated protein (LAP), and a latent TGF-b-binding protein (LTBP). Active TGF-b is released from the latent complex that was activated via cleavage by proteases and other molecules. The activated TGF-b then becomes a ligand for TGF-b type I and II receptors, leading to receptor Smad (R-Smad) phosphorylation, which subsequently binds to the common-partner Smad (co-Smad), and becoming Smad complexes. The Smad complexes translocate into the nucleus and combine with several transcription factors, thereby becoming a transcriptional active complex that activates target genes transcription. In Abbreviations AHR, airway hyper-responsiveness; BAMBI, BMP and activin membrane-bound inhibitor; BK, bradykinin; BMP, bone morphogenetic protein; CCL2/MCP-1, chemokine (CC motif) ligand 2/monocyte chemotactic protein-1; COPD, chronic obstructive pulmonary disease; CRS, chronic rhinosinusitis; CysLT, cysteinyl leukotriene; FoxP3, forkhead box P3; LAP, latency-associated protein; LTBP, latent TGF-b-binding protein; miR, microRNA; PG, prostaglandin; RORc, RAR-related orphan receptor C; TGF-b1, transforming growth factor-beta 1.Allergy 69 (2014) 699-707

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Section: Other Pathwaysmentioning

confidence: 99%

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Yang

Zhang

Feng

et al. 2014

Allergy

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“…New publications have shown that in the nasal cavity, normal mucosa expresses B1 regardless of trigger. 5,6 Moreover, upregulation of B1 in smooth muscles can be found regardless of inflammation. 24 Zhang et al 25 have shown a possible “cross-talk” between the expression of the 2 receptors and that B1 expression may be downregulated by B2 activation.…”

Section: Discussionmentioning

confidence: 99%

Down‐Expression of Kinin Receptors in Allergic Nasal Polyps Epithelia: An Immunohistochemistry Study

Warman

Lahav

Huszar

et al. 2020

Otolaryngol.--head neck surg.

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Objectives To investigate the expression of B1 and B2 receptors in patients with nasal polyps (NPs) compared to controls. Study Design Retrospective case series. Settings Single academic center. Subjects and Methods Nasal biopsies of patients with NPs were compared to inferior turbinates of control patients. Comparisons included basic demographics and comorbidities, intensity of inflammation, and immunohistochemical staining of B1 and B2 receptors measured by immunohistochemistry staining scores (ISSs). Results A total of 41 patients were enrolled, with 21 patients (51.2%) in the NP group and 20 patients as controls. No differences were found in the prevalence of allergic comorbidities and smoking between the groups. The NP group demonstrated significantly higher prevalence of moderate and severe mononuclear infiltrates compared to the control group (57.1% vs 5.3%, P < .001). The NP group had significantly lower B1 expression in smooth muscle compared to the control group (mean ISS 0.22 vs 1.56, P < .001, respectively) and significantly more B2 expression in epithelial cells (mean ISS 1.81 vs 0, P < .001, respectively). Conclusion Patients with NPs exhibit different expression patterns of B1 and B2 compared to control patients. This implies that bradykinin receptor regulation participates in the pathogenesis of NPs.

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“…Microarray hybridization experiments on total RNA extracted with TRIzol reagent (Ambion), were performed at Coriell Insitute for Medical Research, Camden, NJ. The Affymetrix Gene-Chip Human Genome HG-U133A_2 hybridization platform (Affymetrix, Santa Clara, CA) was performed as described previously 30 . Prior to hybridization, RNA was reverted to cDNA using the NuGen Ovation RNA-Seq System V2 (NuGen Technologies, San Carlos, CA).…”

Section: Methodsmentioning

confidence: 99%

Glatiramer Acetate modulates ion channels expression and calcium homeostasis in B cell of patients with relapsing-remitting multiple sclerosis

Criscuolo

Cianflone

Lanzillo

et al. 2019

Sci Rep

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To investigate the effects of Glatiramer Acetate (GA) on B cells by an integrated computational and experimental approach. GA is an immunomodulatory drug approved for the treatment of multiple sclerosis (MS). GA effect on B cells is yet to be fully elucidated. We compared transcriptional profiles of B cells from treatment-naïve relapsing remitting MS patients, treated or not with GA for 6 hours in vitro, and of B cells before and after six months of GA administration in vivo. Microarrays were analyzed with two different computational approaches, one for functional analysis of pathways (Gene Set Enrichment Analysis) and one for the identification of new drug targets (Mode-of-action by Network Analysis). GA modulates the expression of genes involved in immune response and apoptosis. A differential expression of genes encoding ion channels, mostly regulating Ca2+ homeostasis in endoplasmic reticulum (ER) was also observed. Microfluorimetric analysis confirmed this finding, showing a specific GA effect on ER Ca2+ concentration. Our findings unveils a GA regulatory effect on the immune response by influencing B cell phenotype and function. In particular, our results highlight a new functional role for GA in modulating Ca2+ homeostasis in these cells.

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Transcriptional activity of genes-encoding kinin B1 and B2 receptors and kinin-dependent genes in nasal polyps

Cited by 9 publications

References 28 publications

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Down‐Expression of Kinin Receptors in Allergic Nasal Polyps Epithelia: An Immunohistochemistry Study

Glatiramer Acetate modulates ion channels expression and calcium homeostasis in B cell of patients with relapsing-remitting multiple sclerosis

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