Sinonasal Surfactant Protein A1, A2, and D Gene Expression in Cystic Fibrosis: A Preliminary Report

2007 ◽  
Vol 137 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Bradford A. Woodworth ◽  
Rachel Wood ◽  
John E. Baatz ◽  
Rodney J. Schlosser
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Nasal Polyposis ◽  
Quantitative Polymerase Chain Reaction ◽  
Surfactant Protein ◽  
Fungal Rhinosinusitis ◽  
Allergic Fungal Rhinosinusitis ◽  
Novel Treatment ◽  
Polymerase Chain

OBJECTIVE: To measure alterations in SPA1, A2, and D gene expression in various forms of inflammatory chronic rhinosinusitis (CRS). STUDY DESIGN AND SETTING: Sinus mucosal biopsies were performed in patients with allergic fungal rhinosinusitis (AFS), CRS with nasal polyposis, cystic fibrosis (CF), and controls. SP mRNA was measured with quantitative polymerase chain reaction. RESULTS: Patients with CF (n = 4) showed significantly increased SPA1 (82-fold), SPA2 (100-fold), and SPD (47-fold) mRNA ( P < 0.05) when compared with controls (n = 5). Patients with CRS with nasal polyposis (n = 5) also demonstrated elevated SPA1 (27-fold), SPA2 (13-fold), and SPD (13-fold). Patients with AFS (n = 7) had increased SPA1 (5-fold), SPA2 (9-fold), and SPD (17-fold), but were not statistically significant. CONCLUSION: SPA1, A2, and D are upregulated in various forms of CRS, but are significantly elevated in cystic fibrosis CRS. SIGNIFICANCE: Understanding the role of SPs in CRS will help develop novel treatment approaches for sinonasal pathoses.

Distinguishing Molecular Features of Allergic Fungal Rhinosinusitis

2018 ◽  
Vol 159 (1) ◽  
pp. 185-193 ◽  
Author(s):  
Matthew A. Tyler ◽  
Caroline J. Padro Dietz ◽  
Chris B. Russell ◽  
Martin J. Citardi ◽  
Shervin Assassi ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Chronic Rhinosinusitis ◽  
Quantitative Polymerase Chain Reaction ◽  
Sinus Surgery ◽  
Type I ◽  
Chain Reaction ◽  
Molecular Features ◽  
Fungal Rhinosinusitis ◽  
Allergic Fungal Rhinosinusitis ◽  
Polymerase Chain

Objective Allergic fungal rhinosinusitis (AFRS) is a clinical subtype of chronic rhinosinusitis with nasal polyps (CRSwNP), characterized by eosinophilic mucin, evidence of fungal elements within the mucin, fungal-specific type I hypersensitivity, and characteristic computed tomography findings. It remains controversial whether AFRS represents a disease with a unique pathophysiology from chronic rhinosinusitis or is merely a severe form of CRSwNP. The goal of this study was to identify molecular features unique to AFRS. Study Design Cross-sectional case-control. Setting Single academic tertiary referral institution. Subjects and Methods Subjects included 86 patients undergoing endoscopic sinus surgery: CRSwNP (n = 34), AFRS (n = 37), and healthy controls (n = 15). Pathway and correlation analyses were performed with whole-genome microarray data for study patients undergoing surgery for recalcitrant chronic rhinosinusitis. Our findings were confirmed with quantitative polymerase chain reaction and immunohistochemical studies. Results AFRS was uniquely characterized by a pronounced association with adaptive T helper 2–associated immune gene expression. AFRS exhibited altered expression of proteins associated with secretory salivary peptides—namely, histatin, a peptide with known antifungal activity in the oral cavity. Furthermore, the expression of histatins correlated negatively with that of type 2 inflammatory mediators. We confirm the decreased expression of histatins in AFRS when compared with CRSwNP by quantitative polymerase chain reaction and localized its expression to a submucosal cell population. Conclusion There exist clear molecular profiles that distinguish AFRS from CRSwNP. This divergence translates into an altered ability to control fungal growth and may in part explain some of the phenotypical differences between CRSwNP and AFRS.

scholarly journals Effect of D-Mannose on Gene Expression of Neuraminidase Produced from Different Clinical Isolates of Pseudomonas aeruginosa

2019 ◽  
Vol 16 (2) ◽  
pp. 0291
Author(s):  
Shehab Et al.
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Antibacterial Agents ◽  
Quantitative Polymerase Chain Reaction ◽  
Clinical Isolates ◽  
Chain Reaction ◽  
Gene Copies ◽  
Different Types ◽  
Polymerase Chain

The present work aimed to investigate the neuraminidase (nan1) gene expression in 32 different clinical isolates of Pseudomonas aeruginosa to explore the role of the enzyme in different types of infection and might give a better understanding of host cell-pathogens interaction. In addition, the effect of monosaccharide D-mannose on neuraminidase gene expression in eight isolates was studied by utilizing a reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results demonstrated that the highest expression of nan1 gene was in otitis samples (208,913.81) which were significantly higher than that from other infections (P < 0.01). While, the concentrations of gene copies obtained from urine, sputum and burns samples were 93,535.34, 92,254.64 and 74,029.63respectively. While the least expression in wound samples (32,017.06). This suggests that neuraminidase in ear samples might be more virulent and invasive followed by that from urine, sputum, burns and wounds samples. The considerable interest of addition D-mannose significantly reduced the rate of neuraminidase activity reached fivefold in some isolates. This indicates that D-mannose down regulates nan1 gene expression. Hence, this sugar could be used in the development of potential new antibacterial agents where it acts as a competitive neuraminidase inhibitors.

scholarly journals Effect of D-Mannose on Gene Expression of Neuraminidase Produced from Different Clinical Isolates of Pseudomonas aeruginosa

2019 ◽  
Vol 16 (2) ◽  
pp. 0291
Author(s):  
Shehab Et al.
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Antibacterial Agents ◽  
Quantitative Polymerase Chain Reaction ◽  
Clinical Isolates ◽  
Chain Reaction ◽  
Gene Copies ◽  
Different Types ◽  
Polymerase Chain

The present work aimed to investigate the neuraminidase (nan1) gene expression in 32 different clinical isolates of Pseudomonas aeruginosa to explore the role of the enzyme in different types of infection and might give a better understanding of host cell-pathogens interaction. In addition, the effect of monosaccharide D-mannose on neuraminidase gene expression in eight isolates was studied by utilizing a reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results demonstrated that the highest expression of nan1 gene was in otitis samples (208,913.81) which were significantly higher than that from other infections (P < 0.01). While, the concentrations of gene copies obtained from urine, sputum and burns samples were 93,535.34, 92,254.64 and 74,029.63respectively. While the least expression in wound samples (32,017.06). This suggests that neuraminidase in ear samples might be more virulent and invasive followed by that from urine, sputum, burns and wounds samples. The considerable interest of addition D-mannose significantly reduced the rate of neuraminidase activity reached fivefold in some isolates. This indicates that D-mannose down regulates nan1 gene expression. Hence, this sugar could be used in the development of potential new antibacterial agents where it acts as a competitive neuraminidase inhibitors.

scholarly journals Cyclo-oxygenase 2, a putative mediator of vessel remodeling, is expressed in the brain AVM vessels and associates with inflammation

2021 ◽  
Author(s):  
Sara Keränen ◽  
Santeri Suutarinen ◽  
Rahul Mallick ◽  
Johanna P. Laakkonen ◽  
Diana Guo ◽  
...  
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Rank Correlation ◽  
Inflammatory Cells ◽  
Vessel Remodeling ◽  
Brain Avm ◽  
Inflammatory Drugs ◽  
Polymerase Chain ◽  
The Brain ◽  
Cox2 Expression

Abstract Background Brain arteriovenous malformations (bAVM) may rupture causing disability or death. BAVM vessels are characterized by abnormally high flow that in general triggers expansive vessel remodeling mediated by cyclo-oxygenase-2 (COX2), the target of non-steroidal anti-inflammatory drugs. We investigated whether COX2 is expressed in bAVMs and whether it associates with inflammation and haemorrhage in these lesions. Methods Tissue was obtained from surgery of 139 bAVMs and 21 normal Circle of Willis samples. The samples were studied with immunohistochemistry and real-time quantitative polymerase chain reaction (RT-PCR). Clinical data was collected from patient records. Results COX2 expression was found in 78% (109/139) of the bAVMs and localized to the vessels’ lumen or medial layer in 70% (95/135) of the bAVMs. Receptors for prostaglandin E2, a COX2-derived mediator of vascular remodeling, were found in the endothelial and smooth muscle cells and perivascular inflammatory cells of bAVMs. COX2 was expressed by infiltrating inflammatory cells and correlated with the extent of inflammation (r = .231, p = .007, Spearman rank correlation). COX2 expression did not associate with haemorrhage. Conclusion COX2 is induced in bAVMs, and possibly participates in the regulation of vessel wall remodelling and ongoing inflammation. Role of COX2 signalling in the pathobiology and clinical course of bAVMs merits further studies.

scholarly journals Type III Collagen is Required for Adipogenesis and Actin Stress Fibre Formation in 3T3-L1 Preadipocytes

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 156
Author(s):  
Mohammad Al Hasan ◽  
Patricia E. Martin ◽  
Xinhua Shu ◽  
Steven Patterson ◽  
Chris Bartholomew
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Type Iii Collagen ◽  
Type Iii ◽  
Actin Stress Fibre ◽  
Matrix Gene ◽  
Gene Transcripts ◽  
Polymerase Chain ◽  
Oil Red O Staining ◽  
Oil Red O

GPR56 is required for the adipogenesis of preadipocytes, and the role of one of its ligands, type III collagen (ColIII), was investigated here. ColIII expression was examined by reverse transcription quantitative polymerase chain reaction, immunoblotting and immunostaining, and its function investigated by knockdown and genome editing in 3T3-L1 cells. Adipogenesis was assessed by oil red O staining of neutral cell lipids and production of established marker and regulator proteins. siRNA-mediated knockdown significantly reduced Col3a1 transcripts, ColIII protein and lipid accumulation in 3T3-L1 differentiating cells. Col3a1−/− 3T3-L1 genome-edited cell lines abolished adipogenesis, demonstrated by a dramatic reduction in adipogenic moderators: Pparγ2 (88%) and C/ebpα (96%) as well as markers aP2 (93%) and oil red O staining (80%). Col3a1−/− 3T3-L1 cells displayed reduced cell adhesion, sustained active β-catenin and deregulation of fibronectin (Fn) and collagen (Col4a1, Col6a1) extracellular matrix gene transcripts. Col3a1−/− 3T3-L1 cells also had dramatically reduced actin stress fibres. We conclude that ColIII is required for 3T3-L1 preadipocyte adipogenesis as well as the formation of actin stress fibres. The phenotype of Col3a1−/− 3T3-L1 cells is very similar to that of Gpr56−/− 3T3-L1 cells, suggesting a functional relationship between ColIII and Gpr56 in preadipocytes.

scholarly journals Modulation of the Tissue Expression Pattern of Zebrafish CRP-Like Molecules Suggests a Relevant Antiviral Role in Fish Skin

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 78
Author(s):  
Melissa Bello-Perez ◽  
Mikolaj Adamek ◽  
Julio Coll ◽  
Antonio Figueras ◽  
Beatriz Novoa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bacterial Infections ◽  
Quantitative Polymerase Chain Reaction ◽  
Tissue Expression ◽  
Interferon Response ◽  
Fish Skin ◽  
Tissue Expression Pattern ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Antiviral Role

Recent studies suggest that short pentraxins in fish might serve as biomarkers for not only bacterial infections, as in higher vertebrates including humans, but also for viral ones. These fish orthologs of mammalian short pentraxins are currently attracting interest because of their newly discovered antiviral activity. In the present work, the modulation of the gene expression of all zebrafish short pentraxins (CRP-like proteins, CRP1-7) was extensively analyzed by quantitative polymerase chain reaction. Initially, the tissue distribution of crp1-7 transcripts and how the transcripts varied in response to a bath infection with the spring viremia of carp virus, were determined. The expression of crp1-7 was widely distributed and generally increased after infection (mostly at 5 days post infection), except for crp1 (downregulated). Interestingly, several crp transcription levels significantly increased in skin. Further assays in mutant zebrafish of recombinant activation gene 1 (rag1) showed that all crps (except for crp2, downregulated) were already constitutively highly expressed in skin from rag1 knockouts and only increased moderately after viral infection. Similar results were obtained for most mx isoforms (a reporter gene of the interferon response), suggesting a general overcompensation of the innate immunity in the absence of the adaptive one.

scholarly journals Decreased Expression of GPER1 Gene and Protein in Goiter

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Raquel Weber ◽  
Ana Paula Santin Bertoni ◽  
Laura Walter Bessestil ◽  
Ilma Simoni Brum ◽  
Tania Weber Furlanetto
Keyword(s):  
Estrogen Receptor ◽  
Quantitative Polymerase Chain Reaction ◽  
Thyroid Tissue ◽  
Chain Reaction ◽  
Normal Thyroid ◽  
Protein Levels ◽  
Protein Expressions ◽  
Polymerase Chain ◽  
G Protein Coupled

Goiter is more common in women, suggesting that estrogen could be involved in its physiopathology. The presence of classical estrogen receptors (ERαand ERβ) has been described in thyroid tissue, suggesting a direct effect of estrogen on the gland. A nonclassic estrogen receptor, the G-protein-coupled estrogen receptor (GPER1), has been described recently in several tissues. However, in goiter, the presence of this receptor has not been studied yet. We investigated GPER1 gene and protein expressions in normal thyroid and goiter using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. In normal thyroid (n=16) and goiter (n=19), GPER1 gene was expressed in all samples, while GPER1 protein was expressed in all samples of normal thyroid (n=15) but in only 72% of goiter samples (n=13). When comparing GPER1 gene and protein levels in both conditions, gene expression and protein levels were higher in normal thyroid than in goiter, suggesting a role of this receptor in this condition. Further studies are needed to elucidate the role of GPER1 in normal thyroid and goiter.

scholarly journals C/EBPα directs monocytic commitment of primary myeloid progenitors

Blood ◽  
2006 ◽  
Vol 108 (4) ◽  
pp. 1223-1229 ◽  
Author(s):  
Dehua Wang ◽  
Jenice D'Costa ◽  
Curt I. Civin ◽  
Alan D. Friedman
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Fold Increase ◽  
Pcr Assay ◽  
Gm Csf ◽  
Specific Effects ◽  
Proliferation And Apoptosis ◽  
Polymerase Chain ◽  
Lineage Markers ◽  
Transcriptional Induction

Abstract C/EBPα is required for generation of granulocyte-monocyte progenitors, but the subsequent role of C/EBPα in myeloid lineage commitment remains uncertain. We transduced murine marrow cells with C/EBPα-estradiol receptor (ER) or empty vector and subjected these to lineage depletion just prior to culture in estradiol with myeloid cytokines. This protocol limits biases due to lineage-specific effects on developmental kinetics, proliferation, and apoptosis. Also, lowering the dose of estradiol reduced activated C/EBPα-ER to near the physiologic range. C/EBPα-ER increased Mac1+/Gr1–/MPO–/low monocytes 1.9-fold while reducing Mac1+/Gr1+/MPOhi granulocytes 2.5-fold at 48 hours, even in 0.01 μM estradiol. This pattern was confirmed morphologically and by quantitative polymerase chain reaction (PCR) assay of lineage markers. To directly assess effects on immature progenitors, transduced cells were cultured for 1 day with and then in methylcellulose without estradiol. A 2-fold increase in monocytic compared with granulocytic colonies was observed in IL-3/IL-6/SCF or GM-CSF, but not G-CSF, even in 0.01 μM estradiol. C/EBPα-ER induced PU.1 mRNA, and PU.1-ER stimulated monocytic development, suggesting that transcriptional induction of PU.1 by C/EBPα contributes to monopoiesis. A C/EBPα variant incapable of zippering with c-Jun did not induce monopoiesis, and a variant unable to bind NF-κB p50 stimulated granulopoiesis, suggesting their cooperation with C/EBPα during monocytic commitment.

scholarly journals THE LEPTIN GENE IS A MARKER FOR THE CELL THERAPY OF METABOLIC SYNDROME

Biomeditsina ◽  
2019 ◽  
pp. 12-22
Author(s):  
N. V. Petrova
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Cell Therapy ◽  
Bone Marrow Cells ◽  
Liver And Pancreas ◽  
A Cell ◽  
Polymerase Chain ◽  
Lep Gene ◽  
The Brain

It is shown that the level of the Lep gene expression is a marker for B/Ks-Leprᵈᵇ/+ mice, which line serves as an optimal model for describing metabolic syndrome (MS) in preclinical studies. Mice were transplanted with cultured isogenic bone marrow cells (BMC) from heterozygous db/+ donors. The recipients were divided into two groups according to an early or advanced stage of MS development. We analyzed the expression of the Lep gene on the 3rd, 8th and 14th day following the administration of stem BMCs in the brain, liver and pancreas cells by polymerase chain reaction (PCR) in real time. The Lep gene expression was evaluated in terms of the number of cDNA copies. According to our data, leptin is a complete regulator of metabolic processes due to its effect on the hypothalamus, which, together with the hippocampus, controls the production of acetylcholine and insulin in the brain. We have proven the role of the Lep gene as a quantitative criterion for evaluating the effi cacy of a cell therapy in MS.

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