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Your search keyword '"Monocyte adhesion"' showing total 340 results
Start Over Descriptor "Monocyte adhesion" Publication Type Academic Journals
340 results on '"Monocyte adhesion"'

15. CX3CL1-Fc treatment prevents atherosclerosis in Ldlr KO mice

Author

Riopel, Matthew, Vassallo, Melanie, Ehinger, Erik, Pattison, Jennifer, Bowden, Karen, Winkels, Holger, Wilson, Maria, de Jong, Ron, Patel, Sanjay, Balakrishna, Deepika, Bilakovics, James, Fanjul, Andrea, Plonowski, Artur, Larson, Christopher J., Ley, Klaus, Cabrales, Pedro, Witztum, Joseph L., Olefsky, Jerrold M., and Lee, Yun Sok

Published
2019
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16. Anandamide Inhibits Vascular Smooth Muscle Migration, Endothelial Adhesion Protein Expression and Monocyte Adhesion of Human Coronary Artery Cells.

Author

Blessing, Elane, Teichmann, Elisa, and Hinz, Burkhard

Abstract

Endocannabinoids have been shown to play a complex role in the pathophysiology of a number of cardiovascular disorders. In the present study, the effects of the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were investigated in human coronary artery smooth muscle cells (HCASMC) and human coronary artery endothelial cells (HCAEC) with regard to potential atheroprotective and anti-inflammatory effects. In HCASMC, AEA showed an inhibitory effect on platelet-derived growth factor-induced migration, but not proliferation, independent of major cannabinoid-activatable receptors (CB1, CB2, TRPV1), while 2-AG left both responses unaffected. In HCAEC, AEA at concentrations of 6 and 10 µM significantly inhibited the interleukin (IL)-1β- and lipopolysaccharide (LPS)-stimulated expression of vascular cell adhesion molecule-1 (VCAM-1) and LPS-induced intercellular adhesion molecule-1 (ICAM-1), again independently of the abovementioned receptors. Corresponding effects were observed to a lesser extent in the presence of 2-AG, in most cases not significantly. The detection of activated phosphoproteins as well as experiments with inhibitors of corresponding signaling pathways suggest that AEA interferes with IL-1β-induced VCAM-1 expression via inhibition of protein kinase B/Akt and Src kinase activation and attenuates LPS-induced VCAM-1 and ICAM-1 expression via inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation. As expected, AEA also led to a significant inhibition of monocyte adhesion to IL-1β- and LPS-stimulated HCAEC, with siRNA experiments confirming the functional role of VCAM-1 and ICAM-1 in this assay. 2-AG showed a comparatively weaker but, in the case of LPS stimulation, still significant inhibition of adhesion. In summary, the results emphasize the potential of AEA as a protective regulator of atherosclerotic and inflammation-related changes in HCASMC and HCAEC and encourage further corresponding preclinical studies with this endocannabinoid. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Selenopeptide nanomedicine ameliorates atherosclerosis by reducing monocyte adhesions and inflammations.

Author

Luo, Zhen, Jiang, Yuxing, Liu, Zimo, Guo, Lamei, Zhang, Li, Rong, Hongtao, Duan, Zhongyu, Liang, Hongwen, Zhang, Aili, Wang, Lei, Yi, Yu, and Wang, Hao

Subjects
SELENOPROTEINS, CELL adhesion, NANOMEDICINE, ATHEROSCLEROSIS, ATHEROSCLEROTIC plaque, RHESUS monkeys, REACTIVE oxygen species
Abstract

Atherosclerosis is an inflammatory disease that may cause severe heart disease and stroke. Current pharmacotherapy for atherosclerosis shows limited benefits. In the progression of atherosclerosis, monocyte adhesions and inflammatory macrophages play vital roles. However, precise regulations of inflammatory immune microenvironments in pathological tissues remain challenging. Here, we report an atherosclerotic plaque-targeted selenopeptide nanomedicine for inhibiting atherosclerosis progression by reducing monocyte adhesions and inflammation of macrophages. The targeted nanomedicine has 2.2-fold enhancement in atherosclerotic lesion accumulation. The oxidation-responsibility of selenopeptide enables eliminations of reactive oxygen species and specific release of anti-inflammatory drugs, thereby reducing inflammation responses of macrophages. Notably, we find the oxidative metabolite of selenopeptide, octadecyl selenite, can bind to P-selectin in a high affinity with a dissociation constant of 1.5 µM. This in situ generated active seleno-species further inhibit monocyte adhesions for anti-inflammation in synergy. With local regulations of monocyte adhesions and inflammations, the selenopeptide nanomedicine achieves 2.6-fold improvement in atherosclerotic plaque inhibition compared with simvastatin in the atherosclerosis mouse model. Meanwhile, the selenopeptide nanomedicine also displays excellent biological safety in both mice and rhesus monkeys. This study provides a safe and effective platform for regulating inflammatory immune microenvironments for inflammatory diseases such as atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2024
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32. Actinidia arguta Extract Containing Myo-Inositol Suppresses TNF-α-Induced VCAM-1 Expression and Monocyte Adhesion to Endothelial Cells via Inhibition of the PTEN/Akt/GSK-3β and NF-κB Signaling Pathways.

Author

Lee, Jangho, Park, Joon, Song, Kyung-Mo, Lee, Yu Geon, and Choi, Hyo-Kyoung

Subjects
*ANTI-inflammatory agents, *NF-kappa B, *BIOLOGICAL models, *IN vitro studies, *MONOCYTES, *CARDIOVASCULAR diseases, *RESEARCH funding, *CELL physiology, *ATHEROSCLEROSIS, *PHOSPHATASES, *CELLULAR signal transduction, *TREATMENT effectiveness, *DESCRIPTIVE statistics, *PLANT extracts, *INOSITOL, *ANTIGENS, *MICE, *GENE expression, *KIWIFRUIT, *ENDOTHELIAL cells, *ANIMAL experimentation, *GENE expression profiling, *TRANSFERASES, *COMPARATIVE studies, *CELL differentiation, *TUMOR necrosis factors, *PHOSPHOPROTEINS, *DIETARY supplements, *PHARMACODYNAMICS
Abstract

The primary inflammatory process in atherosclerosis, a major contributor to cardiovascular disease, begins with monocyte adhering to vascular endothelial cells. Actinidia arguta (kiwiberry) is an edible fruit that contains various bioactive components. While A. arguta extract (AAE) has been recognized for its anti-inflammatory characteristics, its specific inhibitory effect on early atherogenic events has not been clarified. We used tumor necrosis factor-α (TNF-α)–stimulated human umbilical vein endothelial cells (HUVECs) for an in vitro model. AAE effectively hindered the attachment of THP-1 monocytes and reduced the expression of vascular cell adhesion molecule-1 (VCAM-1) in HUVECs. Transcriptome analysis revealed that AAE treatment upregulated phosphatase and tensin homolog (PTEN), subsequently inhibiting phosphorylation of AKT and glycogen synthase kinase 3β (GSK3β) in HUVECs. AAE further hindered phosphorylation of AKT downstream of the nuclear factor kappa B (NF-κB) signaling pathway, leading to suppression of target gene expression. Oral administration of AAE suppressed TNF-α–stimulated VCAM-1 expression, monocyte-derived macrophage infiltration, and proinflammatory cytokine expression in C57BL/6 mouse aortas. Myo-inositol, identified as the major compound in AAE, played a key role in suppressing THP-1 monocyte adhesion in HUVECs. These findings suggest that AAE could serve as a nutraceutical for preventing atherosclerosis by inhibiting its initial pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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