scholarly journals MicroRNA‐34a in coronary heart disease: Correlation with disease risk, blood lipid, stenosis degree, inflammatory cytokines, and cell adhesion molecules

2021 ◽  
Author(s):  
Hefei Li ◽  
Mingchao Chen ◽  
Qiang Feng ◽  
Lin Zhu ◽  
Zhichao Bai ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Cell Adhesion Molecules ◽  
Disease Risk ◽  
Blood Lipid

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
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