Naturally occurring cell adhesion inhibitors

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Abstract

This paper reviews naturally occurring cell adhesion inhibitors derived from a plant, microbial and marine origin. Plant-derived inhibitors are classified according to a type of structure. Microbially and marine-derived inhibitors were described according to age. In addition, effects of inhibitors on cell proliferation and that of standards on cell adhesion are listed as much as possible.

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Most cited references 79

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Leukocyte-endothelial adhesion molecules.

J Harlan, T. Carlos (1994)

In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of "anti-adhesion" therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.

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Cutting edge: a small molecule antagonist of LFA-1-mediated cell adhesion.

Paul A T Kelly, Lisa Rothlein, Meredith D McNeil … (1999)

LFA-1 (CD18,CD11a) is a cell-adhesion molecule that mediates critical immunological processes. In this paper we report the discovery and characterization of (R)-5-(4-bromobenzyl)-3-(3, 5-dichlorophenyl)-1,5-dimethylimidazolidine-2,4-dione (BIRT 377), an orally bioavailable small molecule that interacts specifically with LFA-1 via noncovalent binding to the CD11a chain and prevents LFA-1 from binding to its ligand, ICAM-1. BIRT 377 inhibits lymphocyte activity both in vitro and in vivo, in functional assays that require LFA-1-mediated cell adhesion. These results demonstrate that LFA-1-mediated leukocyte adhesion can be antagonized with noncharged, low m.w. molecules and suggest that the potential therapeutic value of adhesion inhibitors can be attained with a small, orally bioavailable compound.

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Luteolin protects against vascular inflammation in mice and TNF-alpha-induced monocyte adhesion to endothelial cells via suppressing IΚBα/NF-κB signaling pathway.

Zhenquan Jia, Palanisamy Nallasamy, Dongmin Liu … (2015)

Vascular inflammation plays a significant role in the pathogenesis of atherosclerosis. Luteolin, a naturally occurring flavonoid present in many medicinal plants and some commonly consumed fruits and vegetables, has received wide attention for its potential to improve vascular function in vitro. However, its effect in vivo and the molecular mechanism of luteolin at physiological concentrations remain unclear. Here, we report that luteolin as low as 0.5 μM significantly inhibited tumor necrosis factor (TNF)-α-induced adhesion of monocytes to human EA.hy 926 endothelial cells, a key event in triggering vascular inflammation. Luteolin potently suppressed TNF-α-induced expression of the chemokine monocyte chemotactic protein-1 (MCP-1) and adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), key mediators involved in enhancing endothelial cell-monocyte interaction. Furthermore, luteolin inhibited TNF-α-induced nuclear factor (NF)-κB transcriptional activity, IκBα degradation, expression of IκB kinase β and subsequent NF-κB p65 nuclear translocation in endothelial cells, suggesting that luteolin can inhibit inflammation by suppressing NF-κB signaling. In an animal study, C57BL/6 mice were fed a diet containing 0% or 0.6% luteolin for 3 weeks, and luteolin supplementation greatly suppressed TNF-α-induced increase in circulating levels of MCP-1/JE, CXCL1/KC and sICAM-1 in C57BL/6 mice. Consistently, dietary intake of luteolin significantly reduced TNF-α-stimulated adhesion of monocytes to aortic endothelial cells ex vivo. Histology shows that luteolin treatment prevented the eruption of endothelial lining in the intima layer of the aorta and preserved elastin fibers' delicate organization as shown by Verhoeff-Van Gieson staining. Immunohistochemistry studies further show that luteolin treatment also reduced VCAM-1 and monocyte-derived F4/80-positive macrophages in the aorta of TNF-α-treated mice. In conclusion, luteolin protects against TNF-α-induced vascular inflammation in both in vitro and in vivo models. This anti-inflammatory effect of luteolin may be mediated via inhibition of the NF-κB-mediated pathway.

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Author and article information

Contributors

Satoshi Takamatsu:

ORCID: http://orcid.org/0000-0001-5620-6196

+81-3-3784-8190 , stakamat@pharm.showa-u.ac.jp

Journal

Journal ID (nlm-ta): J Nat Med

Journal ID (iso-abbrev): J Nat Med

Title: Journal of Natural Medicines

Publisher: Springer Japan (Tokyo )

ISSN (Print): 1340-3443

ISSN (Electronic): 1861-0293

Publication date (Electronic): 19 May 2018

Publication date PMC-release: 19 May 2018

Publication date (Print): 2018

Volume: 72

Issue: 4

Pages: 817-835

Affiliations

ISNI 0000 0000 8864 3422, GRID grid.410714.7, Division of Natural Medicine and Therapeutics, Department of Clinical Pharmacy, School of Pharmacy, , Showa University, ; 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555 Japan

Author information

Satoshi Takamatsu http://orcid.org/0000-0001-5620-6196

Article

Publisher ID: 1220

DOI: 10.1007/s11418-018-1220-z

PMC ID: 6096546

PubMed ID: 29779172

SO-VID: fba41eea-aaeb-4a49-9a2b-44bf4ce3ce47

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 21 February 2018

Date accepted : 7 May 2018

Funding

Funded by: Scientific Research (C)

Award ID: 15K08002

Award Recipient : Satoshi Takamatsu

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ScienceOpen disciplines: Complementary & Alternative medicine

Keywords: cell adhesion,inhibitor,natural products,lfa-1,icam-1,huvec,pma,lps,tnf-α

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ScienceOpen disciplines: Complementary & Alternative medicine

Keywords: cell adhesion, inhibitor, natural products, lfa-1, icam-1, huvec, pma, lps, tnf-α

Naturally occurring cell adhesion inhibitors

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Most cited references 79

Leukocyte-endothelial adhesion molecules.

Cutting edge: a small molecule antagonist of LFA-1-mediated cell adhesion.

Luteolin protects against vascular inflammation in mice and TNF-alpha-induced monocyte adhesion to endothelial cells via suppressing IΚBα/NF-κB signaling pathway.

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