scholarly journals LncRNA UCA1, miR‐26a, and miR‐195 in coronary heart disease patients: Correlation with stenosis degree, cholesterol levels, inflammatory cytokines, and cell adhesion molecules

2021 ◽  
Author(s):  
Jie Li ◽  
Zhisong Chen ◽  
Xiaoyan Wang ◽  
Haoming Song
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Cell Adhesion Molecules ◽  
Cholesterol Levels

Polymorphisms in the P-selectin (CD62P) and P-selectin glycoprotein ligand-1 (PSGL-1) genes and coronary heart disease

2004 ◽  
Vol 42 (9) ◽  
Author(s):  
Peter Bugert ◽  
Marion Vosberg ◽  
Mathias Entelmann ◽  
Jürgen Jahn ◽  
Hugo A. Katus ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Endothelial Cells ◽  
Heart Disease ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Coding Regions

AbstractP-selectin and its ligand, PSGL-1, are cell adhesion molecules that facilitate interaction of platelets, leukocytes and endothelial cells. Polymorphisms of these genes have been reported to be associated with coronary heart disease (CHD). In the present study, we characterized the entire coding regions of

scholarly journals Gab2 (Grb2-Associated Binder2) Plays a Crucial Role in Inflammatory Signaling and Endothelial Dysfunction

2021 ◽  
Author(s):  
Vijay Kondreddy ◽  
Jhansi Magisetty ◽  
Shiva Keshava ◽  
L. Vijaya Mohan Rao ◽  
Usha R. Pendurthi
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Signaling Pathways ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Crucial Role ◽  
Cell Adhesion Molecules ◽  
Neutrophil Infiltration ◽  
Inflammatory Signaling ◽  
Necrosis Factor Alpha

Objective: In response to inflammatory insult, endothelial cells express cell adhesion molecules and TF (tissue factor), leading to increased adhesion of leukocytes to the endothelium and activation of coagulation. Enhanced coagulation could further exacerbate inflammation. Identifying key signaling molecule(s) that drive both inflammation and coagulation may help devise effective therapeutic strategies to treat inflammatory and thrombotic disorders. The aim of the current study to determine the role of Gab2 (Grb2-associated binder2), which is known to play a crucial role in the signaling evoked by growth factors and antigen receptors, in inflammatory signaling pathways and contributing to vascular dysfunction. Approach and Results: WT (wild type) and Gab2-silenced endothelial cells were treated with TNFα (tumor necrosis factor alpha), IL (interleukin)-1β, or lipopolysaccharide (LPS). Activation of key signaling proteins in the inflammatory signaling pathways and expression of cell adhesion molecules, TF, and inflammatory cytokines were analyzed. Gab2 −/ − and WT littermate mice were challenged with LPS or S pneumoniae , and parameters of inflammation and activation of coagulation were assessed. Gab2 silencing in endothelial cells markedly attenuated TNFα-induced, IL-1β–induced, and LPS-induced expression of TF, cell adhesion molecules, and inflammatory cytokines/chemokines. Gab2 silencing suppressed TNFα-induced, IL-1β–induced, and LPS-induced phosphorylation and ubiquitination of TAK1 and activation of MAPKs (mitogen-activated protein kinases) and NF-κB (nuclear factor kappa B). Immunoprecipitation studies revealed that the Src kinase Fyn phosphorylates Gab2. Gab2 −/− mice are protected from LPS or S pneumoniae –induced vascular permeability, neutrophil infiltration, thrombin generation, NET formation, cytokine production, and lung injury. Conclusions: Our studies identify, for the first time, that Gab2 integrates signaling from multiple inflammatory receptors and regulates vascular inflammation and thrombosis.

scholarly journals Association between Inflammation and Function of Cell Adhesion Molecules Influence on Gastrointestinal Cancer Development

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 67
Author(s):  
Hsiang-Wei Huang ◽  
Cheng-Chih Chang ◽  
Chia-Siu Wang ◽  
Kwang-Huei Lin
Keyword(s):  
Cell Adhesion ◽  
Tumor Microenvironment ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Gastrointestinal Cancer ◽  
Cell Adhesion Molecules ◽  
Immune Cell ◽  
Immune Escape ◽  
Checkpoint Inhibitors ◽  
Cytotoxic T Cells

Gastrointestinal cancer is highly associated with inflammatory processes inducing the release of cytokines from cancer or immune cells, including interferons, interleukins, chemokines, colony-stimulating factors, and growth factors, which promote or suppress tumor progression. Inflammatory cytokines within the tumor microenvironment promote immune cell infiltration. Infiltrating immune, and tumor-surrounding stromal cells support tumor growth, angiogenesis, metastasis, and immunosuppression through communication with inflammatory cytokines and cell adhesion molecules. Notably, infiltrating immune and tumor cells present immunosuppressive molecules, such as programmed death-ligand 1 (PD-L1) and CD80/CD86. Suppression of cytotoxic T cells promotes tumor avoidance of immune surveillance and greater malignancy. Moreover, glycosylation and sialylation of proteins hyperexpressed on the cancer cell surface have been shown to enhance immune escape and metastasis. Cytokine treatments and immune checkpoint inhibitors are widely used in clinical practice. However, the tumor microenvironment is a rapidly changing milieu involving several factors. In this review, we have provided a summary of the interactions of inflammation and cell adhesion molecules between cancer and other cell types, to improve understanding of the tumor microenvironment.

Inflammatory Cytokines and Cell Adhesion Molecules in a Rat Model of Decompression Sickness

2008 ◽  
Vol 28 (2) ◽  
pp. 55-63 ◽  
Author(s):  
Nancy J. Bigley ◽  
Heather Perymon ◽  
Gloria C. Bowman ◽  
Barbara E. Hull ◽  
Harold F. Stills ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Cell Adhesion Molecules ◽  
Decompression Sickness

scholarly journals The influence of deficit of endogenous neuropeptides on the clinical course of coronary heart disease

2017 ◽  
Vol 95 (2) ◽  
pp. 127-131
Author(s):  
Aleksandr V. Dontsov
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Peroxidation ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Inflammatory Cytokines ◽  
Inverse Correlation ◽  
Cholesterol Levels ◽  
Group 2 ◽  
The Relationship ◽  
Reduced Activity

The study is aimed at elucidating the relationship between the blood b-endorphin level in patients with coronary heart disease (CHD) with metabolic syndrome (MS) and cardiovascular risk factors and evaluating the possibility to correct them by dalargin therapy. The study included 123 patients (61 men and 62 women) at the mean age 57.6±5,2 years randomized into 2 groups. The patients of group 1 (n=63) were given the standard treatment, those of group 2 (n=60) additionally received 2 mg/day of dalargin for 10 days (3 courses during 3 months). The group of comparison (n=84) contained 84 CHD patients without MS. Biochemical and immunological characteristics were measured by immunoenzyme and immunochemiluminescent assays before and 3 months after treatment. The study revealed inverse correlation between b-endorphin levels and those of leptin, insulin, cortisol, TNF-a, IL-6, oxidized LDLP, triglycerides (TG), and HDLP cholesterol. Standard therapy resulted in a 6.5% reduction ofinsulin level, 9,4% , 6,1%, and 17,4% reduction of TNF-a , IL-6, TG levels respectively; it increased the HDLP cholesterol level by 10,3% (p<0,05 for all values) but did not change other parameters of interest. Dalargin therapy caused a 32,6% and 17,4%, rise in the b-endorphin and HDLP cholesterol levels but decreased leptin, insulin, cortisol, TNF-a, IL-6, LDLP, and tG levels by 36,1%, 22,4%, 23,9%, 55%, 56,3%, 14% and 27,2% respectively (p<0,001). It is concluded that the decrease of the blood b-endorphin level in the patients with coronary heart disease and metabolic syndrome is associated with enhanced blood atherogenicity, hyperinsulinemia, hypercortisolemia, activation of pro-inflammatory cytokines and lipid peroxidation. Supplementation of conventional therapy with dalargin results in the increased b-endorphin level, enhanced anti-atherogenic effect, reduced activity ofpro-inflammatory cytokines and lipid peroxidation, reduction of leptin, insulin and cortisol levels.

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