scholarly journals Expression of Emotions and Genes: Proinflammatory Gene Expression Rises With Spousal Distress

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 297-297
Author(s):  
Steven Cole ◽  
M Shrout ◽  
Janice Kiecolt-Glaser ◽  
Stephanie Wilson
Keyword(s):  
Gene Expression ◽  
Marital Conflict ◽  
Marital Quality ◽  
Negative Mood ◽  
Task Effects ◽  
Developmental Theories ◽  
Before And After ◽  
Proinflammatory Gene ◽  
Expression Of Emotions ◽  
Proinflammatory Gene Expression

Abstract Marital quality shares ties to inflammation-related conditions like cardiovascular disease and diabetes. Lab-based studies implicate hostility during marital conflict as a mechanism via inflammatory reactivity. However, developmental theories suggest that conflict declines with age. Spousal distress is an important but overlooked context for aging couples as networks shrink and assistance needs increase. To examine the effects of spousal distress on changes in proinflammatory gene expression, 38 adults ages 40-81 witnessed their spouse relive an upsetting personal memory aloud, rated their mood before and after, and provided blood samples at baseline and twice post-task. Those whose negative mood increased more in response to spousal disclosure showed larger elevations in proinflammatory gene expression 40 (p=.022) and 80 minutes (p<.0001) after the task. Effects were robust to race, gender, age, alcohol, smoking, and body mass index. These novel findings identify spousal distress as a key marital context that may escalate inflammation-related health risks.

CCAAT/enhancer binding protein δ regulates glial proinflammatory gene expression

2013 ◽  
Vol 34 (9) ◽  
pp. 2110-2124 ◽  
Author(s):  
Tony Valente ◽  
Marco Straccia ◽  
Nuria Gresa-Arribas ◽  
Guido Dentesano ◽  
Josep M. Tusell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

scholarly journals Histone Deacetylase 7 Promotes Toll-like Receptor 4-dependent Proinflammatory Gene Expression in Macrophages

2013 ◽  
Vol 288 (35) ◽  
pp. 25362-25374 ◽  
Author(s):  
Melanie R. Shakespear ◽  
Daniel M. Hohenhaus ◽  
Greg M. Kelly ◽  
Nabilah A. Kamal ◽  
Praveer Gupta ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Deacetylase ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

Abstract 573: Endothelial α5 Integrins Regulate OxLDL-Induced Fibronectin Deposition, Proinflammatory Gene Expression, and Early Atherosclerosis

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Arif Yurdagul ◽  
Jonette Green ◽  
Wayne Orr
Keyword(s):  
Gene Expression ◽  
Endothelial Cell ◽  
Inflammatory Responses ◽  
Oxidized Ldl ◽  
Focal Adhesions ◽  
Published Data ◽  
Matrix Remodeling ◽  
Proinflammatory Gene ◽  
Fibronectin Deposition ◽  
Proinflammatory Gene Expression

Alterations in extracellular matrix quantity and composition contribute to atherosclerosis, with remodeling of the subendothelial basement membrane to a fibronectin-rich matrix preceding lesion development. Published data from our lab and others demonstrate that endothelial cell interactions with fibronectin prime inflammatory responses to a variety of atherogenic stimuli. However, the mechanisms regulating early atherogenic fibronectin accumulation remain unknown. Work from our group previously demonstrated that oxidized LDL (oxLDL) promotes endothelial proinflammatory gene expression by activating the integrin α5β1, a classic mediator of fibronectin fibrillogenesis. We now show that treating endothelial cells with oxLDL induces fibronectin deposition and inhibiting α5β1 (blocking antibodies, α5 knockout cells) completely inhibits oxLDL-induced fibronectin deposition. While endothelial fibronectin expression remains unchanged, oxLDL robustly stimulates the deposition of endothelial cell-derived fibronectin associated with a significant reduction in intracellular fibronectin. Interestingly, loss of endothelial cell-derived fibronectin, but not plasma fibronectin, prevents integrin α5 localization to focal adhesions, reduces fibronectin fibril length, and inhibits oxLDL-induced VCAM-1 expression. In addition, inducible endothelial-specific deletion of α5 integrins significantly blunts atherosclerotic plaque formation in ApoE knockout mice, suggesting an important role for this integrin in early endothelial activation. Taken together, our data demonstrate that oxLDL stimulates α5 integrin-dependent subendothelial matrix remodeling and endothelial proinflammatory gene expression through the deposition of fibronectin.

Changes in proinflammatory gene expression in human whole blood after contact with UV-conditioned implant surfaces

2019 ◽  
Vol 23 (10) ◽  
pp. 3731-3738
Author(s):  
Sönke Harder ◽  
Elgar Susanne Quabius ◽  
Fabian Meinke ◽  
Christian Mehl ◽  
Matthias Kern
Keyword(s):  
Gene Expression ◽  
Whole Blood ◽  
Human Whole Blood ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

MDS‐associated SF3B1 mutations enhance proinflammatory gene expression in patient blast cells

2020 ◽  
Author(s):  
Daniel A. Pollyea ◽  
Hyun Min Kim ◽  
Brett M. Stevens ◽  
Frank Fang‐Yao Lee ◽  
Chelsea Harris ◽  
...  
Keyword(s):  
Gene Expression ◽  
Blast Cells ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression
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