The adhesion cascade and anti-adhesion therapy: an overview

Sharar, Sam R.; Winn, Robert K.; Harlan, John M.

doi:10.1007/bf00196093

Cited by 44 publications

(25 citation statements)

References 122 publications

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“…The massive current research input will certainly lead to substantial progress in these areas and to significant clinical applications. The results already obtained using monoclonal antibodies to ICAMs and &integrins are highly promising (Gahmberg et al, 1992b;Isobe et al, 1992;Kelly et al, 1994Kelly et al, , 1996Sharar et al, 1995;Connolly Jr et al, 1996). A detailed knowledge of integrin-ICAM interaction in molecular detail is, however, a prerequisite for developing novel reagents affecting adhesion.…”

Section: Discussionmentioning

confidence: 98%

Leukocyte Adhesion

Gahmberg

Tolvanen

Kotovuori

1997

European Journal of Biochemistry

207

191

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Leukocyte adhesion is of pivotal functional importance and this has resulted in extensive research and rapid develonient in the field. Leukocyte adhesion involves members of three molecular families: integrins, members of the immunoglobulin superfatnily and carbohydrate binding selectins and sialoadhesins. Recently, considerable structural information on leukocyte integrins and members of the immunoglobulin superfrtinily of adhesion molecules has been obtained. This fact. combined with the identification of several novel adhesion molecules. has increased our understanding o f how they function at the molecular level. Furthermore, the important issue of how integrins are activated to become adhesive is rapidly advancing,.. It is clearly evident that the knowledge accuniulated from basic research will increasingly be applied in clinical medicine. In this review we focus on two iinportant families of adhesion molecules. Norc. This Review will be reprinted in EJR Kei?cw.\ 1997 which will be av;iil;ible in April I99X.A number of different leukocytes are known and most probably more subgroups will be found concomitantly with the development in typing procedures. 111 addition, the cells rnay represent different stages of differentiation. An individual leukocyte m 11 s t be able to interact with a number of fundamentally different cells. often modified in various ways. and sometimes with the extracellular matrix or foreign microbes. These facts may partially be the reason that many different leukocyte adhesion systems and molecules exist. In addition i t is certainly useful for the organism to have a certain redundancy i n adhcsion molecule expression and function. which could seciire vital functions cven if some adhesion functions are lost or weakened.Cellular immunology used to be largely phenomenal and not inolecular. But with the development of monoclonal antibody and inolecular cloning techniques, combined with the rapid advance in structural elucidation. present day immunology is certainly ii molecular science, and in inany respects in the forefiont of modern biomedical research. In fact, a number of dcvelopinents in other fields of present day biomedical research originate from breakthroughs in iinmunology. and an excellent exaniple is leukocyte adhesion. Although much remains poorly understood, adhesion receptor-ligand interactions are now appreciated to such an extent that much can be applied t o several other areas of research.But research on leiikocytc adhesion is not rewarding only from a basic point of view. Undoubtedly. the large interest in this field steins from iiuinerous potential clinical applications. Many of the iniljor diseases affecting mankind. like cardiovnscular disease. stroke, chronic and iicute inflammations. cancer. malaria, and inany bacterial and viral infections directly involve leukocyte adhesion molecules. Therefore. it comes as no surprise

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Section: Discussionmentioning

confidence: 98%

Leukocyte Adhesion

Gahmberg

Tolvanen

Kotovuori

1997

European Journal of Biochemistry

207

191

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“…Leukocyte capture and rolling comprise the first phase of this process (150). This stage is mediated primarily by the selectin family of adhesion molecules.…”

Section: Inflammatory Events In Endothelial Cellsmentioning

confidence: 99%

Estrogen and Cerebrovascular Physiology and Pathophysiology

Pelligrino

Galea

2001

Japanese Journal of Pharmacology

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ABSTRACT-Numerous studies have uncovered a wide variety of estrogen effects with apparent cardiovascular benefits, the most recognized ones being vasodilation, anti-atherogenesis, diminished post-ischemic inflammation and anti-oxidant effects. This article provides an overview of the influence of estrogen on the cerebral vasculature, under physiologic and pathophysiologic conditions, and covers both acute and chronic effects. The discussion is primarily focused on the vasodilatory and anti-inflammatory actions of estrogen, since those particular estrogen influences have received the greatest attention in studies published to date. With respect to vasodilation, although some consideration is given to the role of other vasodilating mechanisms and factors, the emphasis is mostly placed on the endothelial isoform of nitric oxide synthase, eNOS, which has emerged as a clear target of estrogen. Some consideration is given to recent findings that suggest that estrogen can stimulate eNOS activity by decreasing the expression of the eNOS inhibitor caveolin-1. With regard to the ability of estrogen to counteract inflammation, potential mechanisms by which estrogen limits the post-ischemic leukocyte adhesion, and the expression of the inducible NOS, are discussed.

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“…In many rodent models of inflammation, tissue injury or other insults generate thrombin, histamine, oxygenderived radicals, or other mediators that stimulate endothelial cells to redistribute P-selectin from Weibel-Palade bodies to the cell surface (67)(68)(69). Depending on the specific challenge, TNF-␣, IL-␤, or LPS may also be elaborated.…”

Section: Figmentioning

confidence: 99%

Tumor Necrosis Factor-α- or Lipopolysaccharide-induced Expression of the Murine P-selectin Gene in Endothelial Cells Involves Novel κB Sites and a Variant Activating Transcription Factor/cAMP Response Element

Pan

Xia

Yao

et al. 1998

Journal of Biological Chemistry

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Tumor necrosis factor-␣ (TNF-␣) or lipopolysaccharide (LPS) increases expression of the P-selectin gene in murine, but not in human, endothelial cells. These mediators augment expression of a reporter gene driven by the murine, but not the human, P-selectin promoter in transfected endothelial cells. The regions from ؊593 to ؊474 and from ؊229 to ؊13 in the murine P-selectin promoter are required for TNF-␣ or LPS to stimulate reporter gene expression. Within these regions, we identified two tandem B elements, a reverse-oriented B site and a variant activating transcription factor/cAMP response element (ATF/CRE), that participate in TNF-␣-or LPS-induced expression. The tandem B elements bound to NF-B heterodimers and p65 homodimers, the reverse-oriented B site bound to p65 homodimers, and the variant ATF/CRE bound to nuclear proteins that included activating transcription factor-2. Mutations in each individual element eliminated binding to nuclear proteins and decreased by 20 -60% the TNF-␣-or LPSinduced expression of a reporter gene driven by the murine P-selectin promoter in transfected endothelial cells. Simultaneous mutations of all elements further decreased, but did not abolish, induced expression. Cooverexpression of p50 and p65 enhanced murine P-selectin promoter activity in a B site-dependent manner. These data indicate that the B sites and the variant ATF/CRE are required for TNF-␣ or LPS to optimally induce expression of the murine P-selectin gene. The presence of these elements in the murine, but not the human, P-selectin gene may explain in part why TNF-␣ or LPS stimulates transcription of P-selectin in a species-specific manner.

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The adhesion cascade and anti-adhesion therapy: an overview

Cited by 44 publications

References 122 publications

Leukocyte Adhesion

Leukocyte Adhesion

Estrogen and Cerebrovascular Physiology and Pathophysiology

Tumor Necrosis Factor-α- or Lipopolysaccharide-induced Expression of the Murine P-selectin Gene in Endothelial Cells Involves Novel κB Sites and a Variant Activating Transcription Factor/cAMP Response Element

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