Effector Functions of Endothelium in Inflammatory and Immunologic Reactions

Wallis, Wayne J.; Harlan, John M.

doi:10.1159/000157005

Cited by 28 publications

(2 citation statements)

References 110 publications

(133 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Endothelial cells are located strategically between blood and extravascular tissue and participate in a variety of inflammatory and immune reactions [52], Clearly, endothelial cells and mips share many common antigens, and therefore it is not surprising that they share common functions, such as the expression of class II antigens, asso ciated with the ability to present antigen [13,14,53,54], MAbs that react with both mips and endothelial cells are of particular interest since they may mark as yet unidenti fied common antigens between these two cell types, such as cell-cell adhesion receptors. The possibility that the anti gens recognized by the mAbs described in this study may be important in some of these endothelial-leukocyte interac tions is under active investigation in our laboratory.…”

Section: Discussionmentioning

confidence: 99%

Monoclonal Antibodies Defining Shared Human Macrophage-Endothelial Antigens

Koch¹,

Burrows²,

Domer³

et al. 1992

Pathobiology

View full text Add to dashboard Cite

We have selected several monoclonal antibodies (mAbs) produced using human rheumatoid arthritis (RA) synovial macrophages (mφs) as immunogen. Of these, mAbs 8H2, 10G7 and 10G9 showed cross reactivity with endothelium, suggesting common antigens between these cell types. We have determined the spectrum of reactivity of these mAbs on hematopoietic cell lines, peripheral blood cells, and inflammatory and non-inflammatory tissues by immunohistochemistry. MAb 8H2 does not react with the myeloid cell lines HL60 (myelocytic), U937 (histiocytic lymphoma), and K562 (erythroleukemia), or with peripheral blood cells. In normal and inflamed tissue sections, MAb 8H2 reacts with mφs and endothelial cells. In contrast, mAb 10G7 does not react with peripheral blood cells, but reacts with HL60, U937, and K562 cell lines, as well as with mφs and endothelial cells in inflamed and nonin-flamed tissues. MAb 10G9 does not react with myeloid cell lines, but reacts with monocytes and platelets in peripheral blood. In both normal and inflamed tissues, MAb 10G9 reacts with mφs and endothelial cells. The antigens identified by these three mAbs were characterized biochemically, by enzymatic digestion of RA synovial tissue mφs followed by a cellular ELISA, as well as by reactivity of the mAbs with NIH-3T3 cells genetically engineered to express known myeloid antigens. These mAbs reacted with protein or glycoprotein antigens distinct from the known myeloid antigens CD 13, CD 14, CD33, CD34, CD36, and c-fms. These mAbs should prove to be a valuable tool for studying mφs and endothelial cells and their shared antigenic determinants.

show abstract

Section: Discussionmentioning

confidence: 99%

Monoclonal Antibodies Defining Shared Human Macrophage-Endothelial Antigens

Koch¹,

Burrows²,

Domer³

et al. 1992

Pathobiology

View full text Add to dashboard Cite

show abstract

“…1 Studies using cultured endothelial cells have provided abundant evidence that the endothelium is involved in all aspects of immunologically and nonimmunologically mediated vascular inflammation. 2 Autoimmune endothelial damage or activation offers an attractive explanation for some of the clinical manifestations of pulmonary disease. In this article, we focus on endothelial cell immunopathology, antiphospholipid antibodies and their relationship to clinical problems such as thrombosis, thromboembolic disease, and pulmonary hypertension.…”

mentioning

confidence: 99%

The Endovascular Compartment

D’Cruz¹,

Khamashta²,

Hughes³

1998

Semin Respir Crit Care Med

View full text Add to dashboard Cite

Autoimmune endothelial damage or activation offers an attractive explanation for some of the clinical manifestations of pulmonary disease. Endothelial cells may for example be involved by antibodies directed against the endothelium and/or by cellular immunity. Alternatively, vascular and organ damage may be caused by thrombosis associated with antiphospholipid antibodies. These heterogenous prothrombotic antibodies include the confusingly named lupus anticoagulant as well as antibodies reacting with negatively charged phospholipids which include cardiolipin. In this article, we have focused on endothelial cell immunopathology, antiphospholipid antibodies and their relationship to clinical problems such as thrombosis, thromboembolic disease and pulmonary hypertension.

show abstract

Enhancement of thrombin‐ and lonomycin‐stimulated prostacyclin and platelet‐activating factor production in cultured endothelial cells by a tumor‐promoting phorbol ester

Zavoico

Hrbolich

Gimbrone

et al. 1990

Journal Cellular Physiology

View full text Add to dashboard Cite

Tumor-promoting phorbol esters such as 4 beta-phorbol 12-myristate 13-acetate (PMA) have been shown to act synergistically with Ca2+ ionophores in cell activation, including stimulation of arachidonic acid metabolism. The effects of PMA on unstimulated and Ca2+ ionophore- or thrombin-stimulated PGI2 and platelet-activating factor (PAF) production in cultured bovine aortic endothelial cells (BAEC) and human umbilical vein endothelial cells (HUVEC) were investigated. Incubation of BAEC or HUVEC for 5-10 min with 100 nM PMA alone slightly increased basal PGI2 production. PGI2 production was rapidly stimulated in BAEC and HUVEC treated with the Ca2+ ionophore ionomycin. Preincubation of BAEC or HUVEC with 100 nM PMA for 5-10 min followed by ionomycin for up to 60 min enhanced PGI2 production up to 2.5-fold. Pretreatment with 100 nM PMA for 5 min also caused a 2-fold enhancement of thrombin-stimulated (1 U/ml) PGI2 production in HUVEC. The production of other prostaglandins, PGF2 alpha, PGE2, and PGD2, was also enhanced. In contrast, PMA had no effect on PGI2 synthesized directly from exogenous arachidonic acid or PGH2. The inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate was without effect. Since the biosyntheses of both PGI2 and PAF share a common first step, the hydrolysis of their respective phospholipid precursors by phospholipase A2, we investigated whether PMA preincubation could also enhance PAF biosynthesis. Incubation of HUVEC with 100 nM PMA alone had a negligible effect on PAF production. However, thrombin-stimulated (1 U/ml) PAF production was enhanced 2.6-fold by preincubation with 100 nM PMA. The protein kinase C inhibitors H-7 and staurosporine ablated the enhancing effect of PMA on thrombin-stimulated PGI2 and PAF biosynthesis. These results demonstrate that PMA can significantly alter the production of PGI2 and PAF in vascular endothelial cells, and suggest that protein kinase C activation modulates phospholipase A2 activity in this cell type.

show abstract

Effector Functions of Endothelium in Inflammatory and Immunologic Reactions

Cited by 28 publications

References 110 publications

Monoclonal Antibodies Defining Shared Human Macrophage-Endothelial Antigens

Monoclonal Antibodies Defining Shared Human Macrophage-Endothelial Antigens

The Endovascular Compartment

Enhancement of thrombin‐ and lonomycin‐stimulated prostacyclin and platelet‐activating factor production in cultured endothelial cells by a tumor‐promoting phorbol ester

Contact Info

Product

Resources

About