85-kDa cytosolic phospholipase A2 group IVα gene promoter polymorphisms in patients with severe asthma: a gene expression and case-control study

Background: Impaired healing after rotator cuff repair is a major concern, with retear rates as high as 94%. A method to predict whether patients are likely to experience poor surgical outcomes would change clinical practice. While various patient factors, such as age and tear size, have been linked to poor functional outcomes, it is currently very challenging to predict outcomes before surgery. Purpose: To evaluate gene expression differences in tissue collected during surgery between patients who ultimately went on to have good outcomes and those who experienced a retear, in an effort to determine if surgical outcomes can be predicted. Study Design: Case-control study; Level of evidence, 3. Methods: Rotator cuff tissue was collected at the time of surgery from 140 patients. Patients were tracked for a minimum of 6 months to identify those with good or poor outcomes, using clinical functional scores and follow-up magnetic resonance imaging to confirm failure to heal or retear. Gene expression differences between 8 patients with poor outcomes and 28 patients with good outcomes were assessed using a multiplex gene expression analysis via NanoString and a custom-curated panel of 145 genes related to various stages of rotator cuff healing. Results: Although significant differences in the expression of individual genes were not observed, gene set enrichment analysis highlighted major differences in gene sets. Patients who had poor healing outcomes showed greater expression of gene sets related to extracellular matrix production ( P < .0001) and cellular biosynthetic pathways ( P < .001), while patients who had good healing outcomes showed greater expression of genes associated with the proinflammatory (M1) macrophage phenotype ( P < .05). Conclusion: These results suggest that a more proinflammatory, fibrotic environment before repair may play a role in poor healing outcome. With validation in a larger cohort, these results may ultimately lead to diagnostic methods to preoperatively predict those at risk for poor surgical outcomes.

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Molecular cloning of rat cDNA for cytosolic phospholipase A2 and the increased gene expression in the dentate gyrus following transient forebrain ischemia [Molecular Brain Research 25 (1994) 364–368]

Molecular Brain Research ◽

10.1016/0169-328x(94)90023-x ◽

1994 ◽

Vol 27 (2) ◽

pp. 355 ◽

Cited By ~ 2

Author(s):

Y. Owada ◽

T. Tominaga ◽

T. Yoshimoto ◽

H. Kondo

Keyword(s):

Gene Expression ◽

Phospholipase A2 ◽

Dentate Gyrus ◽

Molecular Cloning ◽

Brain Research ◽

Cytosolic Phospholipase A2 ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Cytosolic Phospholipase ◽

Molecular Brain

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Lack of Association between Monocyte Chemoattractant Protein-1 (MCP-1) Gene Promoter Polymorphism and Behcet’s Disease with and without Ocular Involvement in Iranian Population: A Case–Control Study

Current Eye Research ◽

10.1080/02713683.2021.1963785 ◽

2021 ◽

pp. 1-5

Author(s):

Maryam Ghaffari Laleh ◽

Mortaza Bonyadi ◽

Elham Shahriyari ◽

Mohammad Hossein Jabbarpoor Bonyadi ◽

Masoud Soheilian ◽

...

Keyword(s):

Case Control Study ◽

Gene Promoter ◽

Promoter Polymorphism ◽

Case Control ◽

Ocular Involvement ◽

Monocyte Chemoattractant Protein 1 ◽

Monocyte Chemoattractant ◽

Monocyte Chemoattractant Protein ◽

Control Study ◽

Gene Promoter Polymorphism

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Cannabis-Dependence Risk Relates to Synergism between Neuroticism and Proenkephalin SNPs Associated with Amygdala Gene Expression: Case-Control Study

PLoS ONE ◽

10.1371/journal.pone.0039243 ◽

2012 ◽

Vol 7 (6) ◽

pp. e39243 ◽

Cited By ~ 28

Author(s):

Didier Jutras-Aswad ◽

Michelle M. Jacobs ◽

Georgia Yiannoulos ◽

Panos Roussos ◽

Panos Bitsios ◽

...

Keyword(s):

Gene Expression ◽

Case Control Study ◽

Case Control ◽

Cannabis Dependence ◽

Control Study

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Enhancement of Cortisol-Induced 11β-Hydroxysteroid dehydrogenase Type 1 Expression by Interleukin 1β in Cultured Human Chorionic Trophoblast Cells

Endocrinology ◽

10.1210/en.2005-1626 ◽

2006 ◽

Vol 147 (5) ◽

pp. 2490-2495 ◽

Cited By ~ 35

Author(s):

Wenjiao Li ◽

Lu Gao ◽

Yan Wang ◽

Tao Duan ◽

Leslie Myatt ◽

...

Keyword(s):

Gene Expression ◽

Phospholipase A2 ◽

Mrna Expression ◽

Reporter Gene ◽

Reductase Activity ◽

Hydroxysteroid Dehydrogenase ◽

Cytosolic Phospholipase A2 ◽

Trophoblast Cells ◽

Cytosolic Phospholipase

Chorion is the most abundant site of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression within intrauterine tissues. It is important to study the regulation of 11β-HSD1 expression in the chorion in terms of local cortisol production during pregnancy. Using real-time PCR and enzyme activity assay, we found that cortisol (1 μm) and IL-1β (10 ng/ml) for 24 h significantly increased 11β-HSD1 mRNA expression and reductase activity in cultured human chorionic trophoblasts. A further significant increase of 11β-HSD1 mRNA expression and reductase activity was observed with cotreatment of cortisol and IL-1β. To explore the mechanism of induction, 11β-HSD1 promoter was cloned into pGL3 plasmid expressing a luciferase reporter gene. By transfecting the constructed vector into WISH cells, an amnion-derived cell line, we found that cortisol (1 μm) or IL-1β (10 ng/ml) significantly increased reporter gene expression. Likewise, an additional increase in reporter gene expression was observed with cotreatment of cortisol and IL-β. To explore the physiological significance of 11β-HSD1 induction in the chorion, we studied the effect of cortisol on cytosolic phospholipase A2 and cyclooxygenase 2 expression. We found that treatment of chorionic trophoblast cells with cortisol (1 μm) induced both cytosolic phospholipase A2 and cyclooxygenase 2 mRNA expression. We conclude that cortisol up-regulates 11β-HSD1 expression through induction of promoter activity, and the effect was enhanced by IL-1β, suggesting that more biologically active glucocorticoids could be generated in the fetal membranes in the presence of infection, which may consequently feed forward in up-regulation of prostaglandin synthesis.

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